Editorial: What Is Special About The Gene?

VOLUME 4, NUMBER 1 (APRIL 2008) SPECIAL ISSUE: WHAT IS SPECIAL ABOUT THE GENE?
GUEST EDITORS: ANDREW EDGAR & STEPHEN PATTISON
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Genomics, Society and Policy 2006, Vol.3, No.2
Contents
Guest Editorial by ANDREW EDGAR & STEPHEN PATTISON Articles What is special about the gene? A literary perspective by DAVID AMIGONI Hybrid Vigour? Genes, Genomics, and History by ROBERTA BIVINS When biology goes underground: genes and the spectre of race by TIM INGOLD The Meanings of the Gene and the Future of the Phenotype by LENNY MOSS Genes and the conceptualisation of language knowledge by ALISON WRAY
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Author Biographies
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Genomics, Society and Policy 2008, Vol.4, No.1, pp.ii-iii
Editorial: What is special about the gene?

The gene may be yesterdays concept as far as science is concerned. However, it is still alive in the popular imagination. It presents a rich challenge to humanities disciplines in generating ideas and analytic perceptions. Furthermore, as the gene and genomics escape the laboratory into everyday life and culture, they shape, and are shaped by, the world views of ordinary people. This in turn modifies the responses of individuals and groups as they engage with scientific and social developments and policies. While much of the discourse about genes and genetics beyond the laboratory is conducted in the language of decision-related and procedural ethics, or that of social analysis, there is a need to stand back and consider how deep, but not necessarily critically-articulated metaphors and understandings are constructed and affect the nature of perceived, taken-for-granted reality. In response to this challenge, a symposium was organised in September 2007 by the Centre for Applied Ethics at Cardiff University. The event emerged from co-operative work between the Centre for Applied Ethics, Cardiffs School of Religious and Theological Studies, and Birmingham Universitys Centre for Global Ethics, on a project entitled The Meanings of Genetics. This project explores the relationship between humanities disciplines and genetics. It asks what the humanities could contribute to understandings of genetic science and technology, and the manner in which these might be interpreted in, and impact upon, contemporary culture. It also attempts to engage with the challenges and opportunities that genetics and genomics pose for the humanities in terms of their methodologies and understandings of human being. A first symposium was organised in 2006, and its papers have already been published in Health Care Analysis. 1 Collected here are the contributions to the second symposium, where scholars from philosophy, history, English literature, cultural anthropology and linguistics, together with a poet, addressed the question: What is special about the gene? Three key themes emerge from the symposium papers and discussions. First, it is clear that the old issues of genetic determinism and the nature/nurture debate continue to trouble humanities scholars, amongst others. In the present collection of papers, the contrasting approaches of linguist Alison Wray and anthropologist Tim Ingold in their respective papers are significant. While Wray explores the possibility that there may be genetic determinants to linguistic capacities, and that such determinants would have significant implications for educational policy, Ingold questions the coherence of the nature-nurture dichotomy, and thus the very possibility of a consistent notion of genetic determinism. Philosopher Lenny Mosss exploration of competing concepts of the gene, and the indeterminism that holds between genotype and phenotype, adds to the consideration of this problem. A second, related theme concerns the politics of genetics and in particular the politics of identity. Genetics potentially challenges our understanding of who we are, and of
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our history. In Hybrid vigour? Genes, genomics, and history, Roberta Bivins explores the impact that genetics will have upon the methodology of the historian, suggesting that the gene and genome can be understood as a source of historical information. This store may never replace more orthodox historical data sources, but it may increasingly become an important complement to them, not least as ordinary people increasingly understand themselves as genetic beings. The final theme concerns the different ways in which the gene and genome are understood by scientists, humanities scholars, and the lay public. The papers herewith illustrate the diverse methods and conceptions, together with rhetorical and metaphorical structures, to which the different humanities disciplines appeal in order to articulate the gene and its place in human culture. This problem is addressed most directly by David Amigoni in his reading of Ian McEwans novel Saturday. He begins to figure the ways in which humanistic and artistic cultures can engage with the cultures of the natural sciences. However, the possible misunderstandings and ambiguities that exist between scientific and humanistic approaches to the gene remain to be explored adequately. Further symposia could fruitfully bring natural scientists and clinicians together with humanities scholars more directly. One contribution to the symposium that is not included in this volume are the poems of Michael Symmons Roberts. He offered readings from his collections Raising Sparks and Corpus. 2 Symmons Roberts worked with Sir John Sulston when he was sequencing the genome. Moved by its beauty and poeticism, he has produced a number of poems relating genetics to love poetry. So, for example, in a tribute to John Donne, Mapping the Genome, he reworks the metaphor of the lover mapping geographically the terrain of their beloveds body in terms of the mapping of the beloveds genome itself. This kind of endeavour begins significantly to bridge the gap that may exist between scientific and lay understandings of the gene, possibly opening up dialogue and public understanding. The symposium demonstrated the urgent need for the humanities to engage with and explore genetics and genomics, as genetic understandings become increasingly part of lay cultures, and thus shape the frameworks, for good or ill, within which contemporary selves, communities and histories are understood. We hope to organise follow-up events, and would be pleased to receive any comments and expressions of interest in this work. Andrew Edgar School of English Communications and Philosophy, Cardiff University Stephen Pattison Department of Theology and Religion, Birmingham University
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Y. Egorova. Editorial, Health Care Analysis 2007; 15 (1): 1-3. M. Symmons Roberts. 1999. Raising Sparks. London: Jonathan Cape; M. Symmons Roberts. 2004. Corpus. London: Jonathan Cape.
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What is special about the gene? A literary perspective

DAVID AMIGONI 1 Abstract In answering the question 'what is special about the gene' from a literary perspective, the article suggests that if literary appreciation is often seen as a mark of human exceptionalism, knowledge of the gene may undermine this claim. Tracing some of the historical and philosophical complexities that circulate around the word 'gene', the article argues that in one sense 'the gene' plays the lead role in the latest 'story' about heredity to preoccupy novelists, scientists, and the literary and cultural historians who have researched their shared interests and mutual borrowings. Reading Ian McEwan's recent novel Saturday (2005) in terms of the traditions of scientific and literary discourse that it draws upon and weaves together, the article argues that the literary craft may yet pose a distinctive challenge for the understanding of the place of genetics and literature in contemporary culture. Introduction Literature, it may be argued, is the form of expression par excellence both for claiming and exploring human exceptionalism. Genetics, on the other hand, may turn out to be the science, par excellence, which debunks the claim to human exceptionialism. As Matt Ridley narrates in his book Nature Via Nurture (2003), in the late 1960s, the work of Vincent Sarich and Allan Wilson indicated that close to 99% of the DNA in the human being is identical to that of a chimpanzee. The work of Roy Britten in 2002 reduced the scale of the difference to around 5%. Even so, the fact that we are, genetically, 95% like a chimpanzee is of little comfort. 2 To think that Bishop Samuel Wilberforce taunted T.H. Huxley at the British Association for the advancement of Science, Oxford, in 1860 at the prospect of the latters being a mere 50% of simian descent. 3 How can literature speak to genetics, and genetics to literature? Of course, this question has, in a sense, already been answered, having been posed again and again: expressiveness has played no small part in the history of encounters between the evolutionary sciences and the seemingly softer pursuits of philosophy and theology as modes of literary discourse. This paper will survey some of the key ways in which the conversation has been, and is being, conducted (Section 1). It will explore the insistent philosophical and ideological complexities that condition literature as an historically self-aware tradition of discourse in dialogue with disciplines and fields that constitute and demarcate objects of scientific knowledge. Of course, as the critical realist Roy Bhaskar would argue, genetics is part of the intransitive ontological domain which exists independently of human activity. But in so far as knowledge of the gene is elaborated by scientific research, then, as critical realism also recognises, the gene is a multi-faceted object of knowledge, entering into the transitive domain of human understanding that is both perspectival and saturated with multiple traditions of discourse and human activity. 4 The dialogic work
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performed by literature reminds us that the intellectual life of the gene that is to say the gene as a conceptual object disseminated by intellectual activity is grounded in discourses, fictions (in their broadest sense), and culture. The article will read Ian McEwans Saturday (2005) a literary fiction as a dialogic act which explores the gene at the interface between what Bhaskar refers to as transitive and the intransitive domains (Section 2). McEwan is a novelist who interrogates the relationship between genetics as an ontological necessity, and the traditional literary and philosophical frameworks that have sustained and validated accounts of human specificity and distinctiveness. 1. Literature and Science: historical and philosophical perspectives What marginal effects do human genes play to make us human, rather than chimpanzee, and what is a gene anyway? Matt Ridley identifies seven meanings of the word gene, and seven different functions few of which contribute decisively to human exceptionalism. First, a gene may be conceived as a Dawkinsian survival machine, using any genomic structure as a host for preserving itself on into the next generation; it is also a Mendelian archive, preserving an ancestral past in the living organism, based on a Watson-Crick recipe of DNA replicators. All of these theories and functions build on De Vriess early sense of heredity conducted by pangens (hereditary material reused in different developmental programmes). A clearer degree of human specificity is made possible by the Jacob-Monod theory of the gene as a developmental switch, a means of promoting and enhancing a particular characteristic in a given bodily design; this also links, perhaps, to the medical theory of the gene as a health-giver, ensuring a healthy outcome in the expected environment. Finally, the theory of the evolutionary psychologists Tooby and Cosmides embraces all of the above, and has come to see the gene as a device for extracting information from the environment. The gene is not, it seems, wholly deterministic. The decisively human part of us continues to be made by our exchange of information with the environment what we have become used, perhaps, to describing as the work of culture. 5 If the gene has multiple functions, it is also hard to be definite about its borders and boundaries. As Richard Dawkins admits in his classic The Selfish Gene it is not easy, indeed it may not even be meaningful, to decide where one gene ends and another begins. 6 Dawkins makes this comment as he describes the process of looking through a microscope at the 46 (23 pairs) human chromosomes, with genes strung out along them in order. Dawkinss observation continues to shape research, almost thirty years after its original publication. In a recent article about gene autonomy, Niall Dillon surveyed a history of the concept of the gene in making this opening point: Rediscovered in 1900 from the research of Gregor Mendel (18221884), and named in 1909 by Wilhelm Johannsen (1857-1927), the gene became one of the most influential scientific concepts of the 20th century. Yet despite its iconic power, it remains a curiously nebulous entity that defies easy definition. From the start, there was a tension between the concept of the gene as a unit of inheritance
which was defined in purely operational terms as an autonomous unit that transmits specific traits through multiple generations and the gene as a physical entity whose position could be mapped in relation to other genes on the chromosome. 7 Dillons work contributes to the critical-realist aspirations of much scientific research: acknowledging genes as a necessary part of ontological reality, while recognising that knowledge of that reality is historically relative and subject to refinement and elaboration. I want to explore some of the tensions produced by this process of refinement and elaboration: the gene as either absolute determinant, or receptor; the gene as either autonomous unit of inheritance or real physical entity. Both point to a certain degree of play at work in the making of the concept of the gene. It is significant that Dillon should go back to the moment of naming of the gene by Wilhelm Johannsen; and that he refers to the iconic power of the concept of the gene. Ill explore this power in relation to what the philosopher Howard Caygill has referred to as the culture of the gene, a transitive culture of metaphysical fictions that needs to be distinguished from the expert, professional day-to-day field work that constitutes molecular biology and biochemistry as it seeks to research more deeply into the intransitive domain. Ill use this to show how another fiction by Ian McEwan, his recent novel Saturday, intervenes into this culture of the gene. 8 It is an intervention that at once venerates the contexts of discovery of modern genetics, yet which also interrogates the force of various mobilisations of the literary in that culture. Turning to the literary, one can note that the power of textual analogy plays a strikingly important role in the conceptualisation of modern genetics. In Darwins Dangerous Idea (1995) Daniel Dennett grasped the workings of the Mendelian archive, the Library of Mendel, by analogy with a textual and philological analogue that followed Borgess imaginary Library of Babel. The literary and textual analogues structure the way in which Roy Britten arrived at his conclusion that humans differ from chimpanzees by virtue of 5% of their DNA. He draws on the language of codes and substitutions. As Ridley points out, Britten identifies the textual deletions and insertions that increase the scale of the difference from 1 to 5%; prior to Brittens work, molecular biologists had only focused on substitutions ie, letters in the text that are different between human and chimpanzee genes. 9 Dawkinss Selfish Gene also uses bibliographic metaphors to describe chromosomes, the copying mechanism of DNA, and Mendelian laws of inheritance. The language of code, and the acts of copying, deleting, insertion may be comfortingly recognisable to literary scholars as the very objects and concerns of their own scholarly pursuits. But only some literary scholars would recognise themselves in such a set of analogies: for instance, bibliographers and historians of the book. That is why Ive added the health warning to my discussion: a literary perspective, for literature is a complex field of critical possibilities and historical legacies. For instance, some literary scholars are theoreticians and deconstructionists; others are historicists. Indeed, it is unnecessary to drive a wedge between them, as many critics bring together a blend between the two, and their work is consequently nuanced and inflected. In any event, all literary criticism needs to be seen in the context of the histories and traditions of
discourse that continue to inform it. Indeed, my reading of McEwans Saturday traces echoes of literary criticisms long historical reflection on the relation between the affective power of poetry and morality, woven into a key moment of narrative crisis sparked by genetic malfunction in one of the novels characters. But the public, justificatory languages of genetic science need to be seen in the same context. Howard Caygill makes the same point about the varied traditions philosophical and scientific thought that inform what he calls the culture of the gene. It is important to stress this variety, complexity and historicity; since the Sokal Affair hoax of 1996, there has been a tendency for leading proponents of the public understanding of science such as the gene theorist Richard Dawkins to homogenise thinking from across the Humanities and Social Sciences negatively as the product of social constuctivism the indefensibly reductive notion that science is just another form of textuality. It is tempting to see a kind of contest at work here between two equally indefensible reductionist drives the postmodern textual and the neo-Darwinian genetic. My own project seeks to move beyond reductionism, both in humanistic and scientific critical pursuits. This tendency to neo-Darwinian reductionism has perhaps pushed many scholars away from a Whiggish present in which the gene dominates, and towards the more varied scientific tapestry of the past. For literary scholars who have explored the literature and science relation, they have focused on it in historically contextual terms. Take my own period of specialisation, the nineteenth century, and its apparent display of a common culture. While the so-called common culture thesis of the social historian of science Robert M. Young can be taken too far, there is something about the intelligibility of nineteenth-century biology that continues to fascinate and in a curious way, perhaps reassure. 10 The disciplines that lent to its formation, at least in its pre-1859 phase geology, comparative anatomy, and classification depended to a large degree on evidence that was available to public display in its primary forms. The molecular biology of genetics is a science that requires not only high degrees of specialisation, and intensive laboratory resources, but depends also on speculative model building that relates to the deeply unseen and unseeable (from Crick and Watsons early 1950s model helices of wood and metal, to computer generated models of molecular activity derived from x-ray crystallography). Lets keep with an historical perspective. What interests literary scholars and cultural historians, and another reason why the effects of the concept of the gene may not be uniquely special to us, is often not so much the validity of the truth claims of the latest scientific theory of inheritance, which is genetics, but the structure and ideological leanings of theories of inheritance from the past. For these theories cast light on the authority of theories at work in the present, and the semantic possibilities and constraints that they offer. In fact, historically-orientated literary scholars are often interested in the languages of inheritance within a scheme of cultural heredity: that is to say where these languages come from, what work they perform, what they pass on, and whether indeed they are passed on at all. We should recall that Charles Darwins own theory of heredity pangenesis that postulated the idea of gemmules that represented every aspect of a body, including acquired characteristics, being transmitted to and out of the sexual organs went precisely nowhere. 11 But pangenesis is fascinating nonetheless for what it says about Darwins interests in
pollen and buds as agents of heredity, and a nineteenth-century idea about the body as a kind of confederated colony of organs. In other words, entangled with the properly delimited scientific speculation about inheritance was a world of discourse about interdependence, and, by implication, politics and governance that resonated more widely in nineteenth-century culture. To give another example: in the 1880s, the German biologist August Weismann formulated his theory of the continuity of the germ plasm. If Darwins theory of natural selection, and Darwins writings in general, could be assimilated to Lamarckian theories of the inheritance of acquired characteristics, Weismanns theory was resolutely anti-Lamarckian. Heredity, for Weismann, was effected by material that was passed reproductively from one generational body to another, but which could not be improved by external influence. Weismanns theory impacted on debates in Europe, in particular debates about degeneration. The English writer Benjamin Kidd in his influential degenerationist tract Social Evolution (1894) used the theory as a basis for concluding that the quality of populations would decline, generation upon generation if natural logics of inheritance were permitted to continue unchecked. Degenerationists such as Kidd argued that the least fit populations, in class terms, were in numerical supremacy, and destined to pass on their unfitness through the germ plasm; acquired characteristics could play no corrective role. For Kidd this necessitated positive action that would ensure and preserve the accumulation of congenital variations above the average to the exclusion of those below in other words, eugenics, which aimed to select certain pools of germ plasm out of the reproductive equation. 12 In one sense, we could dismiss Weismanns theory as superannuated; for instance, in the timeline published on the website of Genome Network News, information supported by the J. Craig Venter Institute, Weismanns work is not cited, so it is not recognised as a milestone on the royal road to the discovery of DNA and the sequence of the human genome. 13 But it is important to recall there are competing stories of intellectual inheritance: to go back to Dawkins again, in his conclusion to the first chapter of the Selfish Gene, he claims that the central idea I shall make use of was foreshadowed by A. Weismann in pre-gene days at the turn of the centuryhis doctrine of the continuity of the germ plasm. 14 Theres a further point to make here about the relationship between eugenics and genetics, a topic that has been compellingly explored in a recent issue of the journal new formations (spring 2007). Im not for a moment suggesting that Dawkins is a eugenicist he is manifestly not but as Hilary Rose argues, there is culturally a connection between genetics and eugenics, and to pretend otherwise is to seek to maintain a soothing fiction. But, she continues, the whole power of soothing fictions lies in their hydra-like reproductive capacities. Cut off their heads and they simply proliferate. 15 Literary and cultural historians are precisely interested in the proliferating fictions associated with science; the reproduction, one might say, of stories about reproduction and inheritance. Lets go back to that formulation of Dawkins in an attempt to illustrate this point: He refers to pre-gene days: how did we get to the naming of genes? When Dawkins refers to pre-gene days, he is referring of course to the days prior to the successes of biochemical experimentation and microscopy that gradually identified the materials of
particulate inheritance that constitute modern genetics. But he is also referring to a movement in scientific nomenclature. The term gene was coined by Johannsen in 1909 a point that Niall Dillon reminds us of in his article about gene autonomy (Nature 2003) during a hectic period when biologists such as De Vries were formulating theories of particulate inheritance while rediscovering the work of Gregor Mendel. Johannsens work performed crucial work in naming the gene, but also those crucial terms in genetics, genotype (the particular genomic plan of the organism), and the phenotype (the particular and variable manifestation in a living individual); and these have important implications for a story told, or as he would put it, drafted about the culture of the gene by the philosopher Howard Caygill. Caygill wrote his Drafts for a Metaphysics of the Gene in 1996. 16 While it may seem to offer a grand narrative about the popularisation of science, its draft status could be said to interrogate, in a productively fragmentary fashion, two crucial philosophical traditions in answering the question what is special about the gene. Those sources are Plato and Nietzsche, the first and last of the metaphysicians for Caygill. In Caygills reading of Nietzsche, science fills the terrible gap left by the death of God in the nineteenth century. Following Nietzsche, Caygill presents science as a Christian substitute, a new Platonism for the masses. Caygills analysis examines the triumph of science in the nineteenth century as a new faith in, and popular culture of, science which reinvented a Platonic Christianity as a metaphysic of science. It was precisely this kind of framework of assumptions that enabled Johannsen to Platonise the late nineteenth-century findings of particulate inheritance into the ideas of the gene, the genotype, and the phenotype a metaphysical legacy that molecular biologists continue to observe yet be troubled by, as a popular culture of genetics demands greater and greater degrees of trust be placed in the metaphysic (your guilt or innocence in a murder case may be determined as true or not by the idea of DNA). Yet it is trust that is bestowed with ambivalence. In twentieth-century genetics, it is the gene that figures as the unstable phenomenon, which at once seems to promise the abolition of nature and chance (the totally engineered subject), while being also the threat of the revenge of chance as it re-enters the order from which, ostensibly, it has been eliminated. In re-reading Plato and Nietszche, Caygills analysis points to another reason why the concept of the gene is not unique: for genetics is just the most recent manifestation of a metaphysical affirmation of science and medicine, ostensibly constituted upon positivist foundations. 17 Caygill also reminds us that it was not only the artists who were expelled from the city in the Republic it was the physicians too, for supplementing nature with their particular brand of techne (much in the way that imitative artists did). The physicians were to be re-admitted in the guise of philosophical legislators. Of course, it may be objected by practising scientists that Caygills narrative is too grand by half, and that he is indulging in social constructivism. But he is careful to distinguish between the nuanced and workaday practices and findings of science, and what he describes as the culture of genetics. Thus, Neither the fear of the abolition of chance in a technical order of necessity, nor the fear of the revenge of chance against the same order have any real basis in the science, but have assumed considerable weight in the culture of genetics. It seems to me that
Caygill implicitly draws a distinction between, to use Hans Reichenbachs terms (subsequently adapted by Christopher Norris), context of discovery, and context of justification, and Bhaskars distinction between intransitive and transitive domains. 18 While fictions of the iconic status of the gene figure in powerful, but carefully circumscribed, ways, literary fictions participate in the culture of genetics in challengingly complex ways. I want to suggest, in conclusion, that Saturday by Ian McEwan an imitative artist who is also deeply attracted by the techne of science and medicine explores the culture of genetics by engaging with the relationship between these transitive and intransitive domains. In a sense, literary narrative can place itself at the exploratory interface between these domains, and their competing claims. For McEwans fictive exploration of the relation between literature and genetics eschews any grand statements about human exceptionalism; in fact, his fiction works to suggest something vaguely disturbing about the human gift for apprehending literature as a mode of affective power, especially in the context of one of the meanings of the word gene: a switch or cultural receptor for mediating information between organism and environment. If the philosophy of critical realism has to be clear and rigorous about the relative stratifications that separate the real, the actual and the empirical, then literature can still be viewed as that privileged space where the blurring of relations between the transitive and intransitive, literature and science, can be exploited as different traditions of discourse clash and meld. 2. Traditions of Discourse in Ian McEwans Saturday: fiction, genetics and poetry Saturday is an urban fiction, a kind of homage to the Modernist literature of the city represented most obviously by Woolfs Mrs Dalloway. 19 It is also possible to see Saturday as a fiction that asks questions about who will legitimately legislate for the city. Of course, in one sense, McEwans evolutionism finds Platonic questions about the governance of the ideal city-state no longer answerable. The governance of the appointed legislators is in one sense farcically detached and ineffective: the central character, a neurosurgeon Henry Perowne, meets Tony Blair at an official engagement, and a distracted Blair mistakes Perownes identity; interestingly, he mistakes him for an artist (Blair is made to comment that a painting mistakenly attributed to Perowne adorns a wall in Downing Street). Saturday stages a confrontation between the two expelled figures from the republic: the artist and the physician. Henry Perowne tends not to intellectualise his working life: a neurosurgeon whose specialisms are at once the molecular biologists knowledge of the micro-composites of life, and the engineers understanding of the body as a complex mechanism. McEwan nonetheless shows him striving to develop an understanding of the affective dimensions of the culture that he inhabits, and a history of the expertise that he contributes to it, through a kind of education orchestrated by his daughter, Daisy. Daisy has read English at Oxford, and is a young published poet: she is determined to educate her father in the literary canon (Flaubert, Tolstoy, Conrad), but also the greats of scientific writing. A recollected image of this reading frames the readers first encounter with the education of Henry Perowne. As Perowne re-awakes on Saturday
morning following his disrupted sleep in the early hours, a phrase passes through his mind: There is grandeur in this view of life. Of course, as he himself comes gradually to realise, this is from Darwin, the closing paragraph of the Origin of Species, unconsciously recalled second hand from the biography that Daisy has set him to study (Daisy conducts her relationship with her father rather in the manner of a tutorial), and read sleepily in the bath the night before. The section of the biography he reads is about the dash to complete the Origin, and a summary of the concluding pages [of the Origin], amended in later editions (p.55). It leads to Perownes reflection on the creation story told by evolution, how out of war, death and destruction, life forms, morality is shaped, and even cities have evolved. Contexts of discovery and contexts of scientific justification seem to mingle together in the verbalised consciousness of Perowne. The evolution of the city, and the illustrious traditions of scientific enquiry that have forged the present, flash through Perownes mind again as he becomes stuck in a traffic jam in London: McEwan sets Saturday on the day in February 2003 when up to a million people took to the streets of London to demonstrate against the impending invasion of Iraq. Perowne tries to take in the scene as it might have been seen by those curious men of the English Enlightenment who gave birth to his world view, and the science that has shaped modern culture. But his attempt to do so is haunted, or in his case thwarted, by literary possibilities that Daisy understands only too well: He tries to see it, or feel it, in historical terms, this moment in the last decades of the petroleum age, when a nineteenth-century device is brought to final perfection in the early years of the twenty first; when the unprecedented wealth of masses at serious play in the unforgiving modern city makes for a sight that no previous age could have imagined. Ordinary people! Rivers of light! He wants to make himself see it as Newton might, or his contemporaries, Boyle, Hooke, Wren, Willis those clever, curious men of the English Enlightenment who for a few years held in their minds nearly all the worlds science. Surely, they would be awed But he cant quite trick himself into it. He cant feel his way past the iron weight of the actual to see beyond the boredom of a traffic tailback He doesnt have the lyric gift to see beyond it hes a realist, and can never escape (p.168). McEwan brings literature and science into cultural contest: Saturday is a day in the life of a professional man on his day off, a fiction that owes much to Woolfs Mrs Dalloway: this moment is an intertextual echo, but so too are Perownes attempts at Modernist epiphanies, Ordinary people! Rivers of light! But its a stand off, the realist surgeon cannot enter into the way of seeing mastered by his lyrical daughter. While Saturday is a novel in which texts that construct and enrich our literacy actually play a significant role, it still poses the question: if we come to know the justification of the neurosurgeons techne (we hear of Perownes skills in the operating theatre, his expertise in molecular biology and bodily engineering), what does literature do, how does it speak within a culture saturated by genetic science? The question begins to be answered as Perowne steers his car away from the jam, and, accidentally, into the path of another car, dislodging its wing-mirror. The minor collision brings Perowne into
the lower social orbit of Baxter and two other petty criminals who use the occasion as an attempt to extort money, and threaten Perowne with a beating when he resists. However, Perowne notes muscular restlessness in Baxters face and, the biochemist and engineer in him immediately reaches this diagnosis: Chromosome four. The misfortune lies within a single gene, in an excessive repeat of a single sequence CAG. Heres biological determinism in its purest form. More than forty repeats of that one little codon and youre doomed. Your future is fixed and easily foretold nightmarish hallucinations and a meaningless end. This is how the brilliant machinery of being is undone by the tiniest of faulty cogs. (p.94) Perowne offers his expert diagnosis, and it turns the situation, exploiting, not the metaphysical, but indeed the magical thinking that hovers below the metaphysical justification of the patient-doctor relationship, and which continues to haunt the legitimating strategies of modern science: They are together in a world not of the medical, but of the magical. When you are diseased, it is unwise to abuse the shaman (p.95). But it is borrowed time, and the episode ends in Baxters humiliation as he loses command of his henchmen, and the moment for violence. Perowne drives off, to a squash match, but will be made to pay. He does so later in the day as the family dinner with Perownes father in law, the poet John Grammaticus, Daisy and his son, is shattered when Rosalind Perowne returns from work with Baxter, his henchmen, and a knife threatening her. It is in this context that McEwan finally answers the question of what literature does. If Perownes magical knowledge of biological determinism shapes the first reversal of Baxters behaviour, then it is a literary recital that shapes the second. Daisy refuses the invaders sexual taunts to read one of her dirty poems from the set of proofs (entitled My Saucy Bark) that sit upon the table; she follows instead Grammaticuss cue and recites Matthew Arnolds Dover Beach, passing it off as her own. What McEwan produces here is a curious kind of parody of literatures civilising mission, so frequently rehearsed in the nineteenth century and since. It seems to me no coincidence that this moment turns on the understanding of an Arnold poem, Arnold being also the author of that great Victorian statement about the civilising mission of literature, Culture and Anarchy (1869). The twitching, simian-like Baxter, wracked by mood swings triggered by faulty genes, becomes a kind of cruelly ironic Arnoldian best self, transformed by a literary conversion. All thoughts of rape dissipate as he says You wrote that its beautiful. You know that, dont you. Its beautiful. And you wrote it. (p.222). The episode is especially rich because of the way in which McEwan translates a lyrical moment into the stuff of storytelling. In narrating the episode, he does not tell that the poem being recited is Dover Beach. The reader oversees fragmented images grasped during the recital from Perownes perspective; Perowne does not know and cannot identify the poem as Arnolds, a further parody, perhaps, of I.A. Richardss experiments with Cambridge undergraduates in the 1920s, exposing them to unidentified poems which they were asked to close-read. Perowne finds many associations, many subject positions from his life and his sense of Daisys life, in the discourse that is recited. McEwan seems to
be suggesting that the civilising process that the poem effects upon Baxter is only one kind of affective response, and ironically it works most powerfully on the most genetically faulty and deranged person present. If the Library of Mendel has inscribed an irrevocable genetic script for Baxter It is written (p.210) the Library of Babel is characterised by indeterminacy. Literature multiplies the positions available for judgement and response. This is hardly a surprising or indeed unsettling conclusion to reach. But McEwans fiction does, I would argue, generate more subtle challenges to received meanings. Indeed, it could be argued that Baxters faulty gene becomes both a switch, and receptor, for the appreciation of poetry, or literature as cultures flagship. Something that begins in genetics, or the intransitive domain of ontological necessity, contributes powerfully to the transitive domain of literary and cultural activity. But it also does so contingently, relatively: that Baxter and Perowne hear such different versions of the poem suggests that there is no universal genetic programme underwriting literary apprehension as some reductive modes of neo-Darwinian have been inclined to argue. 20 We return then to those varied meanings of the gene that Matt Ridley has codified in Nature Via Nurture. McEwans fiction playfully mobilises their varied meanings: the gene as ancestral archive which condemns Baxter to a terrible fate, but also the gene as switch and receptor which precisely generates culture in its profoundly intransitive modes. McEwans fiction, in presenting these different meanings, draws upon historically constituted traditions of discourse. Baxter is made from the naturalist tradition of European fiction, a character determined by heredity, a descendant of the fiction of Gissing and Zola. But he is also touched by those influential discourses of culture and aesthetics that have presented themselves as the antithesis of scientific determinism. In one sense this demonstrates a key claim of this article: that, from a literary perspective, there is nothing particularly special about the gene because it constitutes the most recent episode in a long and inconclusive story about the nature of heredity, the stories that we have inherited about the relations between naturalistic and social inheritance. At the same time, there is of course something wonderfully inventive and distinctive about the particular workings of McEwans fictive exploration of genetics: it does not provide us with unshakeable ground from which to judge the respective claims of the transitive and intransitive domains, in fact it blurs the boundaries between the two. Consequently we have to make meanings out of the contingencies explored by narrative practice. Perhaps this is the point: while Caygill has identified a metaphysical culture of the gene which does indeed exert a powerful and at times ideologically constraining effect in the popular understanding of science, literature as an effect, as a practice exercised by a masterful practitioner such as McEwan, leads us to awkward and conflicting meanings, to be sure: but critical openings, and the antithesis of reductionism.
1 2
English, School of Humanities, Keele University d.amigoni@keele.ac.uk M. Ridley. 2003. Nature Via Nurture: Genes, Experience and What Makes Us Human. London. Fourth Estate. 24-5. I am grateful to the two referees whose comments helped me to re-shape aspects of this argument. 10
For an account see A. Desmond. 1998. Huxley: From Devils Disciple to Evolutions High Priest. Harmondsworth. Penguin. 278-9. 4 For a recent account of the importance of Bhaskars work, and the present state of the critical realist tradition, see, K. Dean, J. Dean & A. Norrie, eds. new formations: critical realism today 2005; 56. 5 Ridley, op. cit. note 2, chapter 9, esp. p.247. 6 R. Dawkins. 1989. The Selfish Gene. 2nd edition. Oxford. Oxford University Press. p.22 7 N. Dillon. Positions Please: On Gene Autonomy. Nature. 2003; 425: 457. 8 Some of the material I use in my reading of Saturday will also appear in a much fuller consideration of McEwan as a novelist who explores scientific ideas, and contemporary scientific culture. See D. Amigoni. The Luxury of Storytelling: science, literature and cultural contest in Ian McEwans narrative practice. S. Ruston (ed.) Literature and Science: Essays for the English Association 2008. Forthcoming. 9 Ridley, op cit. note 2, p.24. 10 See for instance R.M. Young. 1985. Darwins Metaphor. Natures Place in Victorian Culture. Cambridge. Cambridge University Press. 11 A. Desmond & J. Moore. 1990. Darwin. Harmondsworth. Penguin, pp.531-2. 12 B. Kidd. 1894. Social Evolution London. Macmillan, pp.36-7, 192. 13 http://www.genomenewsnetwork.org/resources/timeline/ (consulted 14.12.07) 14 Dawkins, op. cit. note 6, p.11. 15 H. Rose. Eugenics and Genetics: the conjoint twins? new formations: eugenics old and new 2007; 60: 13-26, p.15 16 H. Caygill. 1996. Drafts For a Metaphysics of the Gene. Tekhnema: A Touch of Memory. 3. http://tekhnema.free.fr/3Caygill.htm (consulted 18.06.07) 17 I recognise that positivism is a complex term, and that it is often loosely used by literary and cultural historians. In my account here I implicitly draw on Auguste Comtes nineteenth-century teleological conception of positivism as an integrated approach to both scientific knowledge and social organisation which had moved beyond metaphysics as an evolutionary stage in human development. 18 C. Norris. 1997. New Idols of the Cave: on the limits of anti-realism. Manchester. Manchester University Press, p.5. 19 I. McEwan. 2005. Saturday. London. Jonathan Cape. All further page references to this work will be given in parentheses in the main text. 20 See for instance D.P. Barash & N.R. Barash. 2005. Madame Bovarys Ovaries. New York. Delacorte Press.
11
Hybrid Vigour? Genes, Genomics, and History

ROBERTA BIVINS 1 Abstract Is the gene special for historians? What effects, if any, has the notion of the gene had on our understanding of history? Certainly, there is a widespread public and professional perception that genetics and history are or should be in dialogue with each other in some way. But historians and geneticists view history and genetics very differently and assume very different relationships between them. And public perceptions of genes, genetics, genomics, and indeed the nature and meanings of history differ yet again. Here, in looking at the meaning, and the implications the significance of the gene (and its corollary scientific disciplines and approaches) specifically to historians, I will focus on two aspects of the discourse. First, I will examine the ways in which historians have thus far approached genes and genetics, and the impact such studies have had on the field. There is considerable overlap between the subject matter of genetics/genomics and many of the most widely used analytic categories of contemporary historiography race, gender, sexuality, ethnicity, (dis)ability, among others. Yet the impact of genetics and genomics on society has been studied principally by anthropologists, sociologists and ethicists. 2 Only two historical sub-disciplines have engaged with the rise of genetics to any significant degree: the histories of science and of medicine. What does this indicate or suggest? Second, I will explore the impact of the gene and genetic understandings (of, for example, the body, health, disease, identity, the family, and evolution) on public conceptions of history itself. Decoding genetics: Historical approaches to the gene I confess that from my experience as both an historian and someone who writes a great deal about current work in genetics, I am sceptical, I would even say biased, about claims of a genetic basis for any specific social behaviors. 3 So wrote the renowned historian of biology, Garland E. Allen in 1997. If genetics cannot explain even the social behaviours of individuals, then clearly the gene has little to say about history. And Allens scepticism about the claims made for genetics as an efficient cause or an explanatory system is widely shared by scholars in history, as well as in anthropology, sociology, science studies, and indeed the biological and medical sciences. But historians, particularly of science and medicine, are more than sceptical of the claims of genetic determinists: many are deeply ambivalent or openly apprehensive about what has been called the geneticization of society. Historical studies of genetics reflect and explain their unease. Historians have explored the gene both through studies of its scientific emergence, 4 and through explorations of societal (and economic, and political, and cultural) responses to genetic claims, assumptions, and models of human heredity. 5 Perhaps most disturbingly, historians have examined eugenics movements of the 20th century,
including the role of eugenic thinking in the Holocaust, in forced sterilization campaigns, and in enabling the other tragic outcomes of negative eugenics programmes. 6 Eugenics, whether positive or negative, relied on assumptions that social traits for instance, intelligence, industriousness, honesty, but also stupidity, laziness, and criminality as well as physical ones were biologically inherited, and governed by genes. The commonsense of their day, these assumptions shaped the research designed to test them, and the interpretation of the data produced by those trials. Experiments constructed under these circumstances naturally validated existing beliefs about both marginalized and privileged groups and the evidence they produced was readily accepted as objective despite its poor quality. It is therefore unsurprising that historians like Garland Allen and Daniel Kevles are suspicious of contemporary scientists claims to have found the genes for, say, homosexuality, or criminal violence, and fear that eugenic thought continues to underpin genetic science and genetic medicine. 7 Simply put, historical comparisons suggest ominous similarities between these claims and those of their eugenic predecessors. Other historical approaches have included the study of the gene as a 20th century marker of biological determinism (tainted in historical terms by its use in sociobiology, where biology became destiny in ways profoundly limiting for women, non-whites, and other marginalized groups); and related study of the ways in which genetics could facilitate the construction of a normative biology. 8 Via biography and autobiography, the history of genetics has also yielded exemplary accounts of gender bias in modern science. 9 All in all, existing historical scholarship on the gene and genetics leaves little ground for optimism about the effects of our current cultural fascination with hereditarian, geneticized models of human culture and human history. The idea that our capabilities, our futures, even our souls are encoded in our genes, has historically proven a dangerous one; what risks then are likely to lie in seeking to understand ourselves and our pasts through our genes? In my own historical field, the history of medicine, the impact of the gene and the genetic trope on medical research and practice is clearly visible, if as yet relatively unexplored but the influence of genetic understandings of social, cultural and historical phenomena extends far more widely. As an example to illustrate the problem, consider the congested historical intersection between ideas of race and ideas of biological heredity. Jenny Reardon, working in the field of science and technology studies, has recently demonstrated (coincidentally displaying the traction historians could gain by actively engaging with the anthropological and science studies literatures), the polysemic flexibility and consequent durability of the concept and category race within the scientific disciplines that have focused on heredity, and thus genetics. 10 These traits make it extremely difficult to pin down, moment by historical moment, the meaning of race to scientists and within the scientific literatures. As the science of genetics (and subsequently genomics) gained broader and wider explanatory powers in relation to human variation, race as an explanatory model could disappear linguistically, while persisting intellectually: biological and medical use of race as a category of analysis went, as it were, underground, reinscribed in politically neutral terminology. Thus scientists and medical researchers could retain the analytical power of race without the taint of racism. Many prominent post-war scientists explicitly denied biological race. In severing the direct
connection between the life sciences and racial thought, they also disrupted historical analyses that have been heavily dependent on the language of science, rather than its less accessible and historically documented practices. This neat solution to the problem of race for scientists was pioneered in the 1950s. 11 Today, it persists. On one hand, clinical and research geneticists argue vociferously that self-identified race is only a weak surrogate for a host of more complicated factors in morbidity. 12 On the other, popular, commercial, and indeed some public health models of disease causation often present a far stronger programme, in which biological race determines susceptibility to particular diseases. Even geneticists adamant that race is at best a proxy for authentic sources and markers of genetic difference make assumptions about the (biological and material) nature of those hypothetical authentic signs: On the nongenetic side race carries with it certain social, cultural, educational and economic variables, all of which can influence disease risk. On the genetic side race is an imperfect surrogate for ancestral geographic origin, which in turn is a surrogate for genetic variation across an individual's genome Considered in this context, it is apparent why self-identified race or ethnicity might be correlated with health status, through genetic or nongenetic surrogate relationships or a combination of the two. It is also evident that a true understanding of disease risk requires us to go well beyond these weak and imperfect proxy relationships. And if we are not satisfied with the use of imperfect surrogates in trying to understand hereditary causes, then we should not be satisfied with them as measures of environmental causation either. 13 Collins, the science-trained commentator here, makes several key points. He identifies the flaws in current exclusively genetic models of race and race-linked morbidity, and states that they must be addressed but note his conservatism, and application of the scientific methodology to environmental (in other words, social) causation as well: if we are not satisfied with the use of imperfect surrogates in trying to understand hereditary causes, then we should not be satisfied with them as measures of environmental causation either. History can tell us much about the implications of this kind of gene-thinking, with its stress on absolute certainty and one-to-one correlations of cause and effect. Epidemiological data necessarily often document proxy relationships, and draw attention to indirect, but nonetheless persuasive and relevant links between substances, behaviours and morbidities. Think for example of the long-contested status of the link between smoking and lung cancer. 14 If only perfect data and direct biological links are to be used in health policy making, the public can expect little protection or advice in health matters in the short- or mediumterm. Collins also cautions: If only genetic factors are considered, only genetic factors will be discovered. Historically, the dangers of this approach are all too obvious, as the cases of sickle cell anaemia and thalassaemia illustrate. Sickle cell anaemia (SCA) was first identified as a specific condition in 1910, by Chicago physician James Herrick. 15 As a rare condition prevalent only in underprivileged minority populations,
sickle cell anaemia triggered little clinical or biological interest. By the 1930s, smallscale studies identified the condition as genetically linked, and better defined its pathology, including distinctions between sickle cell disease (SCD) and sickle cell trait (SCT). 16 By this point, the trend of identifying the disease not by its symptoms, but by the cellular phenomenon of sickling was already established, as was a complete identification of the disease with an African origin. 17 Stigmatized in the US as a sign of African-American racial degeneration, the presence of SCA in a family was taken as irrefutable evidence of Negro blood through the 1950s. 18 Even perhaps especially after the specific genetic point mutation that produces SCT/SCA had been identified, racialized stigma remained. What steps are being taken, wrote one British Member of Parliament (well-known for his racist views), to warn the public as a preventive measure that the debilitating genetic disease known as sickle cell anaemia, not present in the indigenous population of Great Britain, can be inherited by the offspring of racially-mixed unions? 19 The same MP sought the segregation of the national blood banks. Only in the 1970s did more nuanced approaches to SCA and other conditions associated with (but not limited to) specific ethnic groups become the norm. 20 Today, we are at risk of slipping backward, of returning to models in which the presence or absence of the genetic mutations associated with sickle cell anaemia or thalassaemia determines race or ethnicity, trumping family history, self-identification, or pluralist ideas of individual heritage and selfhood. And yet the study of the history of genetics has done much for the histories of science and medicine. For example, historians of science concerned with gender (most influentially Evelyn Fox Keller and Donna Haraway) have used molecular genetics and genomics as sites at which to explore the impact of gender on scientific thought, programmes of research, and paradigm-formation. Their work substantially enhanced the credibility of gender as a force in the development (and tool for the exploration) of the scientific professions, and the content of the sciences themselves. In part through this work on the metaphors and constitutive imagery in genetics and genomics, the language of science has been recognized as being more than merely didactic. Rather, it forms and reveals the intellectual structures through and within which scientists conceive their experimental and disciplinary programmes. 21 History may have yet more to gain through tackling geneticization head on; certainly, medical anthropology and medical sociology have captured new audiences particularly in relation to health and science policy through their direct engagement with the impact of genetics and genomics on lay attitudes towards health, risk, and identity. It seems likely that the discipline of history stands to lose at least some of the ground it has gained in terms of inclusivity and accessibility largely through the growth of social history if we ignore the impact of genetics on popular social and cultural understandings of history and the historical. History through a genetic lens: Genes, genomes, geneticists and the human past If the media are to be believed, there is a new kind of history out there, one written and embedded in the human body itself, and just waiting to be read by genetic and genomic scientists. The headline of a 2005 article in the respected UK newspaper The Guardian was blunt: All of human history can be written with four letters. 22 The
body of the article itself reveals the tension inherent in this view. On one hand, it presents DNA as a historical text that reveals a lot about human evolution, and some family secrets, too. But only a sentence or two later, the reporter/protagonist describes the piece of paper which seemingly reveals all: Among the multicoloured lines, the computer-generated graphs and the maps was an innocuous string of letters, beginning, GCTTCTCGCG. This is hardly the transparent window onto the past that one might have expected from the breathless narrative that preceded it. Other accounts, leaning heavily on the traditions of sociobiology, ponder the history of human survival. Under the headline Starch fuel of human evolution, a BBC News story recites a new scientific claim: Man's ability to digest starchy foods like the potato may explain our success on the planet, genetic work suggests. 23 Publicists, like journalists, make much of the power of this new discipline (unlike history based on documents, oral traditions, or even material culture or archaeological finds) to do away with prehistory and the prehistoric. The publishers of one recent book confidently asserted: Historians relying on written records can tell us nothing about the 99.9 per cent of human evolution which preceded the invention of writing. It is the study of genetic variation, backed up by language and archaeology, which provides concrete evidence about the spread of cultural innovation, the movements of peoples the precise links between races. 24 It is worth paying attention to this kind of ephemeral material, I would argue, if only because the use of such claims for mass marketing clearly illustrates the perceived appeal of a scientific, objective, and especially, a complete history. Finally, this genetically inscribed past is presented as a corrective to the errors and biases of its more traditional analogue. Consider, for example the now famous role of genetics in re-writing the history of the third President of the United States of America, Thomas Jefferson. First, in the late 1990s, DNA testing confirmed the oral historical traditions of one branch of the Jefferson clan that they were the descendants of a child born to Jefferson and his slave, Sally Hemings. Unsurprisingly, given US racial politics, these claims had been fiercely denied by Jeffersons white descendants, and ignored as either tendentious or merely contentious by many historical texts and textbooks. It is a powerful indicator of the truth status granted by our society to genetic knowledge that the DNA evidence silenced most (though not all) of the dissenting voices that had dominated debate for over 200 years. 25 As if to confirm claims that human DNA is the archive of this new history, the resources created to test claims of Jeffersonian paternity have now yielded new facts, including a putative Middle Eastern heritage for Jefferson himself: While DNA tests carried out ten years ago famously showed the third US president Thomas Jefferson fathered a child with his slave, Sally Hemings, a new study has found his family comes from the Middle East. Experts at the University of Leicester found Jefferson's Y chromosome belongs to the rare 'K2' class, found in Egypt and
introduced to Britain thousands of years ago. 26 Neither the original article, nor subsequent coverage supplied any interpretation of this new information about Jefferson. Whether this omission suggests that meaning is beyond the remit of genetic history, or that the meaning of the concrete evidence it supplies is or ought to be a truth self-evident is as yet unclear. In each of these examples, we see the gene, or clusters of genes acting as a new kind of historical evidence, for a new kind of history, a history with periodization often closer to that of geology than of social or political history. A rapidly growing body of (largely popular) work propounds this approach. Their titles are revealing: Mapping Human History: Genes, Race, and Our Common Origins; The Great Human Diasporas: The History of Diversity and Evolution; Genes, Memes and Human History: Darwinian Archaeology and Cultural Evolution. 27 This history ignores or downplays the evidence and artifacts of culture in favour of molecular biological evidence. But just like the poorly or incompletely interpreted document, these apparently transparent physical artifacts can easily become meaningless, or even deceitful artifacts in the biomedical, rather than the historical sense. Henry Louis Gates Jr, eminent Harvard scholar of African American literature, and an early enthusiast of the new history, was also an early victim of its flaws. 28 In 2000, having come to the end of the paper trail in his search for the African roots of his own family in other words, having run out of conventional historical sources Gates submitted his DNA for genetic testing, and was promised and then provided with definitive results pinpointing the geographical origins of his ancestors. So far, so good: geneticized history steps in to save the day when historical scholarship fails. Unfortunately, some time later, Gates took another DNA test, and was given different results. Instead of rejecting the approach that had left him with multiple identities, Gates founded a company to do it better, by incorporating more traditional historical methods. When interviewed by the Wall Street Journal on the subject, Gates agreed that the application of genetics to history was problematic; however, he ascribed the problems not to the nature of genetic evidence, but to the reluctance of some companies to reveal the complexity of the results. 29 The names of the companies too are telling: DNA Tribes; African Ancestry; IdentityGenetics, Inc., and Gates own AfricanDNA. Ideas of racial and ethnic identity are at the heart of this new industry. The companies are quite explicit both abut their target consumer groups, and the relationship between their services and history. One corporate spokesperson argued: For most African-Americans, there is no paper trail we make money, but we see this as a service to a people who have been cut off from their history and culture. 30 Surely it behoves historians to examine this phenomenon and ask what analytic categories like race and ethnicity mean in their new context and why they remain so attractive, when the very science that ostensibly underpins genetic history claims that race does not exist as a biological entity. One aspect that immediately strikes the historians eye is the association between the Roots phenomenon of the 1970s (particularly for African Americans) and the emergence of geneticized history. As David Chioni Moore pointed out in 1994,
scholars across the humanities have yet to engage with the social and cultural impact of Alex Haleys novel Roots (and the 1970s television series based on it). 31 As the actor Isaiah Washington noted of his own DNA ancestry test I remember watching Roots when I was young and it stuck with me. I always wanted to know where my ancestors came from before slavery, and here you have the science telling you. 32 Roots sent a generation of African Americans in search of their origins, with new hope that they might find an ancestor, biologically of the same substance, linking them directly and authentically to Africa. The controversies about plagiarism, fictionalized elements, and fabrications that soon surrounded Roots undermined that optimism and highlighted how difficult and dubious historical genealogy could be. Not only does genetic testing seem to offer an easier route to discovering a specific ancestral identity, but that origin is imbued with the same truth status that we as a society grant to scientifically created knowledge of the natural world in general: that of uncontestable fact. Troy Duster, a sociologist who has studied this new marketplace of pasts, noted the impact that such tests can have on their recipients identities: People are making lifechanging decisions based on these tests and may not be aware of the limitations. 33 So why have historians generally ignored this phenomenon in their explorations of the gene, genetics and genomics? Are we threatened by this new history from below (or by the encroachments of science)? Or have genes just become the new germs are we merely reproducing the scientific evangelism of our forebears, who sought a germ for every sickness just as passionately and unreasonably as we seek a gene for every trait? 34 Part of the reason for historical indifference surely lies in the use to which geneticized history is currently being put. In 1942, the American ethnologists E. S. Craighill Handy and Elizabeth G. Handy tore their eyes away from Hawaiian culture long enough to wryly observe their own: As a pleasant and harmless form of antiquarianism, the study of family history, biography, and the tracing of genealogy are tolerantly humoured but certainly not seriously honoured by historians and scientists. [F]amily records are considered of no importance to the larger world of scholarship and science unless related to the lives of distinguished persons. 35 The attitude they observed remains a part of historical culture (although thanks to social history, we have become considerably more enthusiastic about family records, and rather less exclusively concerned with distinguished persons). But it is only a part of the answer. Like many professional historians, I am ambivalent about this newer, truer but also narrower history. Because our society currently gives genetic information such a high truth status, we risk being blinded to persistent assumptions and prejudices if they are clothed in genetic terms. Anthropologists and sociologists are already exemplifying these problems in, for example, studies of the new reproductive technologies, and in medical and forensic genetics, but they are intimately linked, too, with the tools of genetic history. As Duster points out, There is a yet more ominous and troubling element of the reliance upon DNA analysis to determine who we are in terms of lineage, identity, and identification. The very technology that tells us what
proportion of our ancestry can be linked, proportionately, to subSaharan Africa (ancestry-informative markers) is the same being offered to police stations around the [USA] to predict or estimate whether the DNA left at a crime scene belongs to a white or black person. This ethnic estimation using DNA relies on a social definition of the phenotype. ... With the demonstrable skew of the incarcerated population over the last few decades along social categories of race, African-Americans need to be particularly sensitive to the use of phenotype as the starting point for understanding genotype. 36 Under these circumstances, it becomes the job of historians to point out the fact that we are repeating a pattern into which we have slipped before and with no very positive outcome. Phrenological and anthropometric approaches to the modelling of race were also once the acme of modern science, and they have been retrospectively diagnosed as racist sciences; germ theory and eugenic sociobiology were applied to explain every human disease, to the great detriment of those treated with ineffective sera, or stigmatized as unfit to breed (or lives not worth living). Professional historians can also engage with this biological past creatively and productively. We need not simply dismiss it as old wine in new bottles. The gene has heightened the profile of what might called the historical mindset: the idea that the past is connected to the present, shapes it, and also can be revealed by it. While researching this piece, I meandered the far-flung tendrils of the web, looking for the different kinds of connections being made between the constructs gene and history. I was stunned to discover so prominent among them this idea that you could research your family history through genetic testing. But it casts light on a broader problem for the discipline. One difficulty professional historians have had in presenting satisfying representations of the past is not unlike the problem mathematicians and indeed medical geneticists have in explaining risk: just as they say that risk is probabilistic, and thus in individual cases uncertain, we say that history and historical outcomes are contingent and relative. Occams Razor notwithstanding, knowledge-workers tend to enjoy complexity and to see it as signifying a richer and more accurate account of reality. But there is a break in the narrative flow of cause and effect when things get complicated. The new genetic history bridges that chasm, in part by rooting itself so far in the past that the data have already been thoroughly winnowed. Thus another crucial element for historians to observe about the genetic turn in history is that the ascendance of genetic explanations, particularly in relation to human traits and familial morbidity, is a return to narrative albeit a narrative outside of time to all intents and purposes. Here, the past is not erased by progress, as is the ideal in many other sciences and scientific tropes but it is encased in amber, reified, self-replicating, and crucially, linear. This is by no means a justification for writing poorer, simpler, artificially linear history. History is complicated, is contingent, is polysemic we just have to render that complexity comprehensible and satisfying.
19
Acknowledgements I would like to thank the anonymous referees; the speakers and audience who attended the Cardiff University Centre for Applied Ethics 2007 workshop What is special about the gene?; and Mary Wren Bivins for their valuable comments on this piece.
Cardiff School of History and Archaeology, Cardiff University, UK bivinsre@cardiff.ac.uk In particular, those who work in the interdisciplinary nexus of science and technology studies. See for example, K. Finkler. 2000. Experiencing the New Genetics: Family and Kinship on the Medical Frontier. Philadelphia. University of Pennsylvania Press; S. Franklin. 2007. Dolly Mixtures: The Remaking of Genealogy. Durham, VA. Duke University Press; S. Franklin & S. McKinnon, eds. 2001. Relative Values: Reconfiguring Kinship Study. Durham, VA. Duke University Press; H. L. Kaye. 1986. The Social Meaning of Modern Biology: From Social Darwinism to Sociobiology. London: Yale University Press.; J. Reardon. 2005. Race to the Finish: Identity and Governance in an Age of Genomics. Princeton: Princeton University Press; M. Strathern. 1992. Reproducing the Future: Essays on Anthropology, Kinship and the New Reproductive Technologies. New York. Routledge. I should note here also the highly pertinent contributions of geographer Catherine Nash. See C. Nash. Genetic kinship. Cultural Studies 2004; 18 (1): 133, for an excellent review of work specifically addressing genetic kinship, as well as a geographers perspective on the new genetic genealogy I discuss in section 2. 3 G. E. Allen. The social and economic origins of genetic determinism: a case history if the American Eugenics Movement, 1900-1940 and its lessons for today. Genetica 1997; 99: 77-88 (p.78). 4 Exemplars include L. Kay. 2000. Who Wrote the Book of Life? A History of the Genetic Code. Stanford, CA. Stanford University Press; J. Sapp. 1987. Beyond the Gene: Cytoplasmic Inheritance and the Struggle for Authority in Genetics. New York. Oxford University Press. 5 For example, see P. J. Beurton, R. Falk & H.-J. Rheinberger, eds. 2000. The Concept of the Gene in Development and Evolution: Historical and Epistemological Perspectives. Cambridge UK. Cambridge University Press; E. Fox Keller. 1992. Secrets of Life/Secrets of Death: Essays on Language, Gender and Science. New York & London: Routledge. E. Fox Keller. 1995. Refiguring Life: Metaphors of Twentieth-century Biology. The Wellek Library Lecture Series at the University of California, Irvine. New York: Columbia University Press. Here I must also note a approach which has come to my attention too late for inclusion here. Hans-Jrg Rheinberger, Staffan Mller-Wille, and Christina Brandt have in recent years led a series of collaborative workshops aimed at defining 'A Cultural History of Heredity'. One volume of essays arising from this collaboration has now been published: S. Mller-Wille & H.-J. Rheinberger, eds. 2007. Heredity Produced: At the Crossroads of Biology, Politics, and Culture, 1500-1870. Cambridge, MA. MIT Press. Further essays, more specifically related to the gene, are available online as preprint 343 at http://www.mpiwgberlin.mpg.de/en/research/preprints.html. 6 That is, of attempts to improve the human race or breeding stock through eliminating those humans regarded as inferior, or as likely to produce inferior progeny. Negative eugenics is usually contrasted to positive eugenics, which strove to achieve the same ends a better, healthier, and even happier human race via encouraging superior individuals to pair and produce many children. For an intriguing overview of the many different paths of eugenics in the US, see A. Minna Stern. 2005. Eugenic Nation: Faults and Frontiers of Better Breeding in Modern America. Berkeley, CA. University of California Press. 7 Among many examples of this historical approach, see Allen, op. cit. note 3, and M.B. Adams, ed. 1990. The Wellborn Science: Eugenics in Germany, France, Brazil, and Russia. Oxford. Oxford University Press; D.J. Kevles. 1985. In the Name of Eugenics: Genetics and the Uses of Human Heredity. New York. Alfred A. Knopf; D.J. Kevles and L. Hood, eds. 1992. Code of Codes: Scientific and Social Issues in the Human Genome Project. Cambridge MA. Harvard University Press; R.N. Proctor. 1988. Racial hygiene: Medicine under the Nazis. Cambridge, MA. Harvard University Press; N.H. Rafter. 1997. Creating Born Criminals: Biological Theories of Crime and Eugenics. Urbana:
2
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University of Illinois Press; N. Leys Stepan. 1991. The Hour of Eugenics: Race, Gender and Nation in Latin America. Ithaca: Cornell University Press. P. Weindling. Modernising Eugenics. The Role of Foundations in International Population Studies. Minerva 2002; 167-179. 8 For an overview and critique of biological determinism, see S.J. Gould. 1996. The Mismeasure of Man. New York: W. W. Norton; and G. Allen. The Roots of Biological Determinism. Journal of the History of Biology 1984; 17 (1): 141-145. 9 See for example, E. Fox Keller. 1983. A Feeling for the Organism: The Life and Work of Barbara McClintock. San Francisco. Freeman; and compare, A. Sayre. 1975. Rosalind Franklin and DNA. New York. W.W. Norton & Company with J.D. Watson, The Double Helix: A Personal Account of the Discovery of the Structure of DNA (Norton Critical Editions). New York. Norton. 1981 (originally published 1968). 10 See Reardon, op.cit. note 2, esp. her second chapter Post World War II Expert Discourse on Race. For an alternative perspective, see D.B. Paul. 1998. The Politics of Heredity: Essays on Eugenics, Biomedicine, and the Nature-Nurture Debate. Albany: State University of New York Press. 11 Again, see Reardon, op. cit. note 2, who in chapter 2 offers valuable examples form the scientific literature. 12 F.S Collins. What we do and don't know about race, ethnicity, genetics and health at the dawn of the genome era. Nature Genetics 2004; 36 Published online: 26 October 2004. Accessed 08/09/2007 at http://www.nature.com/ng/journal/v36/n11s/full/ng1436.html 13 Ibid. Emphasis added. 14 For a history, see A. Brandt. 2007. The Cigarette Century: The Rise, Fall, and Deadly Persistence of the Product That Defined America. New York. Basic Books; R. Kluger. 1996. Ashes to Ashes: America's Hundred-Year Cigarette War, The Public Health & The Unabashed Triumph of Phillip Morris. Alfred A. Knopf. 15 For a history of sickle-cells biomedical discovery and elucidation, see C. Conley, Sickle-cell anaemia -- the first molecular disease in M. Wintrobe, Blood, Pure and Eloquent: a story of discovery, or people and of ideas, New York, McGraw-Hill, 1980, pp. 319-37. See also K. Wailoo. A disease sui generis: the origins of sickle cell anemia and the emergence of modern clinical research, 1904-1924. Bulletin of the History of Medicine 1991; 65: 185-208. 16 Sickle cell anaemia is now recognized as the homozygous form of a balanced genetic polymorphism (pratically speaking, a trait that exists in multiple forms in a population, each form of which confers some selective advantage). People who are heterozygous for at the sickle cell locus have no symptoms of the disease, but can pass the trait to their children. 17 The symptoms of sickle cell anaemia, as well as the anaemia itself and the painful crises, include capillary engorgement, leg ulcers, infections, thrombosis and a range of long-term sequelae including organ damage. 18 K. Wailoo. 1997. Drawing Blood, Technology and Disease Identity in Twentieth Century America. Baltimore, MD. Johns Hopkins University Press: 134-161; M. Tapper. An anthropathology of the American Negro: anthropology, genetics and the new racial science, 1940-1952. Social History of Medicine. 1997; 10: 263-89. This explanation, of course, fit well with US (and to a lesser degree UK) convictions about the dangers of miscegenation and racial mixing. 19 The Minster of Health answered rather evasively, None. Sickle cell anaemia can occur in children only where both parents carry the necessary mutant gene. See The National Archives (UK) MH159/121. 20 See Wailoo, op. cit. note 15; K. Wailoo. 1997. Drawing Blood Technology and Disease Identity in Twentieth-Century America. Baltimore. The Johns Hopkins University Press; K. Wailoo. 2001. Dying in the City of the Blues: Sickle Cell Anemia and the Politics of Race and Health. Chapel Hill. University of North Carolina Press; M. Tapper. Interrogating Bodies: Medico-Racial Knowledge, Politics, and the Study of a Disease. Comparative Studies in Society and History 1995; 37: 76-93. 21 See for examples, E.Fox Keller. 1992. Secrets of Life, Secrets of Death: Essays on Language, Gender, and Science. New York. Routledge; E.Fox Keller. 2000. The Century of the Gene. Cambridge, MA. Harvard University Press; D. araway. 1997. Modest_Witness@Second_Millenium. Femaleman. copyright Meets_OncoMouse trademark: Feminism and Technoscience. London. Routledge; N. Stepan. Race and Gender: The Role of Analogy in Science. Isis 1986; 77: 261-277. E. Fox Keller. Gender and Science: Origin, History, and Politics. Osiris 1995 (2nd Series); 10: 26-38. For a brief case study of the role of gendered language in shaping experiments in early bacterial genetics (illustrating _____________ Genomics, Society and Policy, Vol.4, No.1 (2008) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com 21
some of the strengths and the weaknesses of the linguistic turn in the history of science), see R. Bivins. Sex Cells: Gender and the Language of Bacterial Genetics. Journal for the History of Biology 2000; 33: 113-139. 22 Alok Jha. All of human history can be written with four letters. The Guardian. April 28, 2005. 23 http://news.bbc.co.uk 10/09/07 24 Cover text, L.L Cavalli-Sforza. 2001. Genes, Peoples and Languages. London. Penguin Press Science. Emphasis added. 25 For a fuller account of this case, including documentary and biological evidence, chronology, and dissenting views, see J.E. Lewis & P.S. Onuf, eds. 1999. Sally Hemings and Thomas Jefferson: History, Memory and Civic Culture. Charlottesville: University Press of Virginia. This example was also disseminated to far wider audiences through the medium of a Public Broadcasting Service television series. See its homepage at http://www.pbs.org/wgbh/pages/frontline/shows/jefferson/ 26 Anonymous. DNA reveals presidents slave child. Rare Match. Metro (30/03/2007). 27 L.L. Cavalli-Sforza. 1995. Great Human Diasporas: The History of Diversity and Evolution. New York. Addison-Wesley; S. Olson. 2002. Mapping Human History: Genes, Race, and Our Common Origins. New York. Houghton Mifflin; S. Shennan. 2002. Genes, Memes and Human History: Darwinian Archaeology and Cultural Evolution. London: Thames & Hudson. 28 R. Nixon. DNA Tests Find Branches But No Roots. New York Times (Business, November 25 2007). 29 K.J. Winstein. Harvard's Gates Refines Genetic-Ancestry Searches for Blacks. Wall Street Journal (November 15,2007), D5. See also C. Elliott and P. Brodwin. Identity and genetic ancestry tracing. British Medical Journal 2002; 325 (7378), 14691471, which responds to the establishment of the first commercial genetic ancestry testing company; and Y. Ergorova & T. Parfitt. 2006. Genetics, Mass Media and Identity: A Case Study of the Genetic Research on the Lemba and Bene Israel. London. Routledge. 30 As quoted in Nixon, op. cit. note 18. See also Nash, op.cit. note 2. 31 D. Chioni Moore. Routes. Transition 1994; 64: 4-21. See N.L. Arnez. From His Story to Our Story: A Review of Roots. The Journal of Negro Education 1977; 46 (3): 367-372, for a contemporary perspective on the phenomenon. 32 Nixon, op. cit. note 18. 33 Nixon, op. cit. note 18. 34 For examples of the publics enthusiastic embrace of the germ, see N. Tomes. 1998. The Gospel of Germs: Men, Women, and the Microbe in American Life. Cambridge, MA. Harvard University Press. 35 E.S. Craighill Handy and E.G. Handy. Genealogy and Genetics. William and Mary Quarterly 1942; 22: 381-388 (p.386). 36 T. Duster. Deep Roots and Tangled Branches. Longview Institute. Accessed 09/12/2008 at www.longviewinstitute.org/research/duster/deeproots
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When biology goes underground: genes and the spectre of race 1

TIM INGOLD 2 Abstract This paper examines the changing meanings of the concept of biology, and of its opposition to culture, through an analysis of the ways in which anthropologists have sought to refute the idea that humanity is divided into distinct races. Efforts to redefine all extant humans as belonging to a single sub-species, or to replace race with culture, only serve to perpetuate raciological thinking. This kind of thinking had its origins in the moral evaluation of physical difference, the construction of hierarchy and essentialist typology. In its 1996 Statement on Race, the American Association of Physical Anthropologists ruled out any connection between the biological and cultural characteristics of human beings. Yet the statement is internally inconsistent in the meanings it attributes to both biology and culture. These shifts in meaning correspond to phases in the history of anthropology, identified here as the Enlightenment phase (culture as a process of civilisation drawing on universal biopsychological capacities), the Consensual phase (culture as diverse traditions inscribed upon a common biological substrate) and the Interactionist phase (behaviour as the product of an interaction between culturally and genetically transmitted information in a given environment). The paper seeks an alternative, relational approach that focuses on the dynamics of developmental systems. Only through such an approach, it is argued, can we wrest biology away from the combination of geneticism and essentialism that continues to perpetuate the logic of raciology even in the course of its vehement denial. Introduction For some years now, and along with many anthropological colleagues, I have been seeking a way of understanding the relations between human beings and their environments that allows us to overcome the separation, so deeply entrenched in western thought and science, between the world of nature and the world of human society. 3 This also means trying to overcome the division in the way we tend to see ourselves, as social beings or persons on the one hand, and as biological organisms, members of a particular species, on the other. The problems we face are formidable. Much of the difficulty stems from the inherent slipperiness of our concepts, and none are more slippery than the concepts of biology and culture. To introduce the problem, I want to begin by unpacking what has surely been one of the most sensitive notions in the whole history of anthropology, namely that of race. Most academic disciplines are proud of their history, and like to trace their origins to the work of great scholars of the past. Anthropologists are less fortunate, for there is no getting around the fact that the discipline owes its origins, very largely, to the virulent racism of the late nineteenth century. 4 There was a period, from around 1870 to 1920, when anthropology quite explicitly identified itself as the study of the different races of mankind. Indeed this is still how the subject is often popularly portrayed. For todays
anthropologists, however, this image is a source of continuing embarrassment. They would like to put it behind them, once and for all. Yet somehow the spectre of race continues to haunt them. One reason for this is obvious: we live in a world in which racism is still rampant, so that as students of society we have to confront the questions of what people mean by race, why the idea still exercises such a hold on the imagination, how it shapes attitudes towards the self and others, and how these, in turn, bear upon the experience of social life. But there is another reason which, for anthropologists, is rather less comfortable. It is that the arguments they have used to refute the idea that humanity is divided into distinct races still carry with them the germs of the very kind of thinking they claim to demolish. 5 By and large, anthropologists have tried to deal with the problem of race in two ways. The first is by declaring that all humankind comprises just one race or sub-species, Homo sapiens sapiens, all other sub-species (such as the ill-fated Neanderthals) having long since been reduced to extinction. But does this amount to an acknowledgement that race does not exist? Far from it. To say that all humans are of one race is not to dismiss the concept of race itself, but rather to confirm it. It is to claim not just that race exists, but that in the prehistoric past though no longer today there were indeed distinct races of mankind. The story that is told by modern science, of how superior creatures of our own race, Homo sapiens sapiens (or anatomically modern humans, as they are known by specialists), spreading north from Africa, overran the continent of Europe at the expense of its indigenous Neanderthal population, is almost a precise mirror image of the nineteenth century story of the how white Europeans were destined to colonise and subjugate the primitive races of black Africa. 6 What the new story has in common with the old is the belief in a shared essence, or common human nature, that makes us what we are, coupled with the notion that this essence is passed on genealogically that is, by descent. Nor is this combination of essentialism and genealogical thinking in any way shaken by the second way in which modern anthropology has tackled the problem of race, that is by simply replacing the word race with the word culture. Instead of saying that humanity is divided into distinct races, anthropological orthodoxy swung to the view that it is divided into distinct cultures, superimposed upon a human nature that is common to all. 7 But the logic of this division remains precisely the same; only the mechanism of genealogical transmission has been changed from genetic inheritance to social learning. Thus the reasons that anthropologists latterly adduced for the existence of separate cultures namely, that the members of a culture share a common essence or heritage that is passed on by descent would, if applied in the realm of biological variation, lead straight back to the existence of race. The problem for contemporary anthropology is that any critique of the concept of race that would really carry conviction would, at one and the same time, have to be a critique of the concept of culture as well. We cannot have it both ways, both rejecting the idea of race while holding on to the idea that humanity is segmented into discrete cultures. For the reasons why races dont exist are also the reasons why cultures dont exist. 8
From race to raciology But I have run ahead of myself. We need to take a step back, to discover how the idea of race came to be so deeply embedded in the political and intellectual milieu within which anthropology first took shape as a distinct discipline. Of course, like all concepts that touch a raw nerve in human history, race has meant many things to many people. Yet for anyone who still believes that concepts are immaterial, or that arguments about concepts are mere word-play for academics, divorced from the struggles of the real world, the invidious role that notions of race have played in the history of humanity must surely prove otherwise. The race concept, as anthropologist Eric Wolf puts it, has presided over homicide and genocide. 9 One might add that the concept of culture has had historical consequences that are scarcely less devastating, as we have seen in recent movements of ethnic cleansing. It is indeed worth reflecting on the reasons why those who are adamant in their rejection of the race concept are nevertheless happy to embrace the concept of culture, on almost exactly the same terms. The etymological source of the word race has been traced albeit somewhat inconclusively to the Latin generare (to beget) and generatio (generation). The root meaning is one of common descent, or shared genealogical origin. It is in this sense that, at least until quite recently, one could often find authors for example of popular travel books talking about the races of men inhabiting this territory or that country, in much the same sense that we might now talk about nations, cultures, peoples or ethnic groups. And in the same sense, race is still popularly used as a synonym for species, as in the human race. Usages of this kind, though perhaps rather loose, are relatively harmless. However in the eighteenth and nineteenth centuries, during the heyday of European colonial expansion, the notion of race gathered additional connotations that converted it from a merely descriptive term into one that carried an exceedingly potent moral and political charge. Roughly speaking, these connotations had their origins in three lines of thought: i) It was supposed that peoples physical appearance or type was an index of their temperament or moral disposition, so that one could read off what people were like good or bad, honest or crafty, intelligent or stupid, active or passive from the way they looked. ii) It was assumed that different types could be arranged in a single hierarchy from inferior to superior, such that higher races would inevitably win out in what came to be seen as a struggle for existence. iii) Every race was thought to represent a type in the strict sense: that is to say, for each race there was supposed to correspond an essential form of the human being Caucasoid, Mongoloid, Negroid, and so on to which every living individual represented a more or less close approximation. These three tendencies the moral evaluation of physical difference, the construction of hierarchy, and essentialist typology were together responsible for the climate of
racism within which the discipline of anthropology emerged and which is now a source of such shame. Modern scholarship, of course, claims to have shown that the underlying assumptions of racist thinking, or of what Wolf calls raciology, 10 have no scientific credibility. First of all, racial essentialism the belief that human beings come in a number of fixed racial types was shown to be incompatible with Darwinian evolutionary theory. Modern evolutionary biologists are concerned not with the enumeration of distinct types but with the mapping of genetic distributions. For any particular gene or characteristic, this map resembles the kind of chart we see every day on the television weather forecast, showing tomorrows expected temperatures. The lines on the chart are contours indicating temperature gradients; they are not absolute boundaries between hot and cold. Likewise, genetic distribution maps use contours to depict graded variations in the percentage of the population that carries a particular character. But for every character you might select, the map looks quite different. If you were to superimpose maps for a range of different characters, then you would find no neat correspondence but an apparently chaotic tangle of intersecting gradients. There is, then, no basis for a division of humankind into defined sub-groups on the basis of hereditary characteristics. This point seems incontrovertible. Moreover there is no evidence to suggest that extant human populations can be ranked in terms of any criterion of superiority or inferiority. Consider for example the hotly disputed criterion of intelligence. Are some populations more intelligent than others? The majority of contemporary anthropologists would, I think, take the view that there is no way of measuring intelligence that is not culture-bound. If children from other cultures do badly in intelligence tests devised by western psychologists and educationalists, this is simply because the ways in which the problems are set, and indeed the whole institutional apparatus of the test with its attendant technologies and authority structures, are alien to their experience. 11 Many anthropologists would probably want to go even further, to claim that the very notion of intelligence is an invention of western discourse, and that it corresponds to nothing real that could be objectively measured. I myself am of this opinion. But let us suppose just for the sake of argument that there is such a thing as intelligence, and that you can use standard testing procedures to measure it. There still remains the question of the extent to which a persons intelligence is a function of genetic inheritance on the one hand, or, on the other, of the environmental circumstances in which he or she was brought up. Again, most anthropologists would be inclined to place more emphasis on nurture than nature, though for my part I think the whole nature/nurture debate is misconceived. (Later on, I shall explain why.) However, even if it really were the case that a persons level of intelligence is genetically determined, that would still not mean that intelligence varied by race. For this to be so there would have to be significant differences in average intelligence between populations. Although suggestions to this effect have been made from time to time, 12 there is no evidence whatever to support them. And even if such evidence could be adduced, it would rest on so many undemonstrable assumptions namely
that intelligence exists, that it can be measured by standard tests, and that it has a significant innate component as to be virtually meaningless. Biology, culture and the statement on race A much more tricky problem, however, turns on the issue of the relation or rather the lack of it between the biological or physical characteristics of human beings and those aspects of morality, temperament and behaviour that are generally bracketed under the rubric of culture. Right from the early decades of the twentieth century, the absolute separation of biological variation and cultural difference has been central to the anthropological refutation of raciology. In 1930 the acknowledged founder of American cultural anthropology, Franz Boas, declared unequivocally that any attempt to explain cultural form on a purely biological basis is doomed to failure. 13 So far as most anthropologists were concerned, that was that. This separation or detachment of the cultural from the biological dimensions of human being effectively split anthropology itself into the two quite distinct divisions of physical (or biological) anthropology on the one hand, and social (or cultural) anthropology on the other. Ever since, biological and sociocultural anthropologists have proceeded quite independently of one another addressing apparently different problems, collecting different kinds of data and speaking different conceptual languages. The present consensus, on both sides of this academic divide, is summed up in the formal statement on race recently adopted by the American Association of Physical Anthropologists. There is, according to this statement, absolutely no connection between the biological and cultural characteristics of human beings. The crucial passage is reproduced in full below: There is no necessary concordance between biological characteristics and culturally defined groups. On every continent, there are diverse populations that differ in language, economy, and culture. There is no national, religious, linguistic or cultural group or economic class that constitutes a race. However, human beings who speak the same language and share the same culture frequently select each other as mates, with the result that there is often some degree of correspondence between the distribution of physical traits on the one hand and that of linguistic and cultural traits on the other. But there is no known causal linkage between these physical and behavioural traits, and therefore it is not justifiable to attribute cultural characteristics to the influence of genetic inheritance. 14 Evidently the intent of the statement is to draw a line under the whole issue: to make it clear, once and for all, that whatever biological differences may exist between people, they are of absolutely no consequence so far as their acquisition of culture is concerned. Unfortunately however, as I shall show, the statement is largely incoherent. And the source of the incoherence lies in fundamental ambiguities surrounding the meanings of both biology and culture. A glance through the recent (and not so recent) literature reveals a host of different senses of biology and the biological, some of them mutually compatible, others
directly contradictory. 15 They can be reduced, however, to five, which I summarise below. Biology can mean: i) ii) iii) iv) v) A focus on the basic capacities and dispositions that humans have in common with other animals (especially non-human primates). A search for what is universal to the human species rather than variable between populations. An emphasis on the behaviour of individuals rather than higher-order social groupings. A Darwinian explanatory paradigm of adaptation under natural selection, or some cultural analogue of the same. A concern with the discovery of genetic, as opposed to learning-transmitted, influences on behaviour.
If we return to the statement on race, it appears to set out from the third of these senses of the biological. Let me pause to explain this sense a little further. It has long been conventional, in social and cultural anthropology, to suppose that the members of a society or community are united by their possession of a common culture that is, by a shared corpus of rules and meanings. The limits of sharing, then, were thought to define the limits of society. Thus culture came to be seen as an essentially collective phenomenon, as a property of a higher-level entity, namely society, with an existence and a form of consciousness of its own, over and above the level in which human beings exist as individual organisms. As everything cultural was, so to speak, creamed off to this higher level, the individual was left as a residually biopsychological entity. From this logic stemmed the idea that biologists and psychologists study individuals, while anthropologists and sociologists study groups. There seems to be something inherently groupy in our thinking about society and culture, and something inherently individualising in our thinking about minds and organisms. 16 And this thinking seems to be confirmed in the first sentence of the passage I cited from the statement on race, which asserts that there is no necessary concordance between biological characteristics and culturally defined groups. If groups are defined by their possession of shared culture, then biological characteristics must belong to individuals. But the statement then carries on to make a distinction between physical traits on the one hand and cultural traits on the other. This is to move to another (and in the history of American anthropology, earlier) notion of culture as a property of individuals, now distinguished from biology in terms of a logic of sameness and difference. 17 Biology is simply taken to mean what all human beings have in common a sort of lowest common denominator for the species as distinct from those characteristics in which they differ. This corresponds to the second of the five senses of the biological listed above. For example, it might be argued that the facial gesture we call the smile is found among all humans everywhere: it is therefore a biological or physical trait. The manual gesture of hand-shaking, on the other hand, is by no means universal, so it is assumed to be a cultural trait. Or again, walking is said to be biological, whereas swimming, skating or cycling is cultural. The identification of the biological with what is universal is, of course, a simple corollary of the assumption that, among humans, all difference is due to culture. However as soon as
we turn to non-human species, which are not supposed to have any culture, that assumption ceases to apply. That is why we end up with the curiously contradictory positions that whereas in the human world, biology is taken to be what makes everyone the same, in the non-human world, biology is supposed to be the source of all variability and difference. The statement then shifts its terms yet again. It speaks of the difference between physical traits and behavioural traits. So culture is now to be read as behaviour. This shift has to be understood in terms of a distinction that is central to the whole explanatory framework of modern biology: between genotype and phenotype. 18 The genotype is an underlying programme for constructing an organism of a certain kind, and is thought to be encoded in the materials of heredity, the genes. The phenotype, by contrast, is what we see: the organism as it actually appears to an observer, situated within a particular environment. There are two dimensions to the phenotype: the morphological (the outward form of the organism, what it looks like) and the behavioural (the activity of the organism, what it is observed to do). Culture, in the sense that currently concerns us, is simply the human phenotype in its behavioural aspect. This identification of culture with the behavioural phenotype paves the way for biology, as it were, to go underground. Rather than referring to phenotypic traits that all humans have in common, it comes to be identified with the genotype, the inner programme at the heart of each human organism, hidden away in the nucleus of every cell of the body. The source of the genotype/phenotype dichotomy lies in the Darwinian theory of variation under natural selection, augmented in the so-called modern synthesis of twentieth century biology through an alliance with population genetics. The logic of the theory rests on the assumption that elements of the genotype alone can be passed from one generation to the next. And it is the genotype that is supposed to evolve through changes in the frequency of its information-bearing elements, the genes. The formation of the phenotype, by contrast, plays no part in the evolutionary process; it is confined within the life-cycle of each individual organism, beginning with its conception and ending with its death. Thus the notion that culture is phenotypic whereas biology is genotypic takes us to the fourth of the senses of biological listed above: the sense that equates biology with a Darwinian (or more strictly, neoDarwinian) perspective. Once, however, biology comes to be identified with the genes, or more specifically with genetic inheritance, the way is opened for an alternative view of culture, not as phenotypic behaviour, but as an underlying programme for behaviour, analogous to the genetic programme but transmitted by an alternative mechanism of inheritance namely, social learning. Hence we arrive at the fifth and final sense of the biological in our list, referring to genetic as opposed to learning-transmitted influences on behaviour. Now it is not just biology that has gone underground, but culture also. A distinction is introduced between culture and behaviour, the former referring to underlying rules and instructions (analogous to the genetic programme), the latter to their outwardly observable effects. To emphasise the analogy with genes, many writers have taken to calling the elements of transmitted culture by the term memes a term coined by biologist and popular science writer Richard Dawkins. 19 Thus the
human being receives, down the line from its ancestors, one set of genetically transmitted programme elements (genes), and another set of learning-transmitted programme elements (memes). And when the statement on race ends by opposing cultural characteristics to genetic inheritance, it draws directly on this notion of culture as intergenerationally transmitted information. Looking at the whole passage from the statement on race, it should now be clear not only that it appeals to several notions of the biological or physical, but also that it continually shifts the goal-posts as regards the definition of culture. First culture is identified as a property of groups (as opposed to individuals), then it becomes a property of individuals (referring to attributes in which they differ rather than those they have in common), and finally it is identified with particles of heritable information that individuals are supposed to carry in their heads, analogous to the genes they carry in their bodies. It is possible to correlate these shifts, albeit rather roughly, with three ways of thinking about the distinction and the relation between biology and culture, that have characterised successive phases in the history of anthropology. I call these the Enlightenment phase, the Consensual phase and the Interactionist phase. In what follows, I shall first outline each of these phases, and then go on to conclude by suggesting how a focus on human development might at last allow us to move beyond the distinction between biological and cultural dimensions of human existence. From civilisation to consensus The Enlightenment phase, dating from the middle of the eighteenth century, was founded on the doctrine of the psychic unity of mankind, according to which all humans are alike in their basic potentials but differ in the degree to which these potentials are realised. From this point of view the biological part of man, otherwise known as human nature, constitutes a universal baseline for cultural development that has taken humanity from its primitive hunter-gatherer past to modern science and civilisation. This was Edward Tylors view, as set out in his monumental Primitive Culture of 1871. It is important to stress that although Tylor was indubitably ethnocentric, in judging every culture by the standards of western civilisation and in placing his own society unequivocally at the top of the scale, he was not or at least not yet racist in his views. Primitive people, he thought, had all the necessary capacities to enable them to be civilised, but these capacities remained unfulfilled. A decade later, however, following the publication of Darwins The Descent of Man, Tylor changed his mind. Darwin had argued that culture could only be as advanced as the brains that produce it. The brains of civilised nations, he thought, were superior to those of barbarous tribes, in the same measure that the latter were superior to the brains of apes. Thus there was no way in which the savage could be educated into civilisation, since his brain simply wasnt big enough to accommodate it. Some advocates of so-called social Darwinism went so far as to argue that, since primitive peoples were destined to lose out in the struggle for existence, the best way to promote the advance of human civilisation was to do everything possible to hasten their demise. This is not, it should be said, a position with which Darwin himself
concurred. Yet it continued to resurface, notably in the eugenics movement, which sought to improve the human race through controlled breeding. 20 It was against this background that anthropologists of the early twentieth century, particularly in the United States, reasserted the independence of culture and race. In 1917 one of the leading anthropologists of the day, Alfred L. Kroeber, published a paper under the title The Superorganic, that established what was to be the anthropological orthodoxy for years to come. 21 Kroeber insisted that cultural phenomena were superorganic in the sense that they existed on a distinct and higher plane of reality with emergent properties of its own. Racial categories could only apply to human beings as biological organisms; they had no purchase on the superorganic world. Today Kroebers work, once enormously influential, is all but forgotten not because his views are no longer accepted but because what needed to be spelled out explicitly then is nowadays part of what most anthropologists simply take for granted. But the reaction, in early twentieth century American anthropology, was not only against racism; it was also against the doctrine of evolutionary progress the idea that the peoples of the world could be ranked on a single scale of absolute advance. Against this, Kroeber and his contemporaries argued that cultures could not be ranked higher or lower on any single scale; they were simply different. And these differences were thought to be imprinted upon a common substrate of biological universals. Man, Kroeber wrote, is a tablet that is written upon: nature provides the tablet, culture the message that is written. 22 That, then, is the foundation for what I call (following Clifford Geertz) the consensual view of the distinction between human biology and culture. 23 In this view, the essence of human nature was to be found not by stripping away the accumulated achievements of culture to reveal the natural man beneath, but rather by factoring out behavioural traits that are apparently common to all human groups. Those traits, for example, that are shared by the Scots, the Japanese and the Australian Aborigines belong to nature, those traits that differ from one group to another belong to culture. Note that this is not equivalent to saying that the Australian Aborigine is somehow closer to nature than the Scotsman. It is not a matter of having more or less culture, or of culture having reached different degrees of development. It is simply a matter of the inscription of different cultural messages upon the same basic substrate. Human nature no more constrains cultural form than paper constrains what you write on it. Interaction and development Kroeber was writing during the heyday of the so-called nature-nurture controversy a controversy that was originally formulated in these terms by Darwins cousin, Francis Galton. In 1874, Galton had published an influential book entitled Engish men of science: their nature and nurture, which purported to show that scientific genius was innate, and could not be accounted for in terms of the quality of upbringing. 24 Others took up the argument on the side of nurture, arguing that the conditions of upbringing were everything, and that heredity could account for nothing at all. Though the debate has carried on furiously for decades, most biologists and anthropologists now take the view that behaviour cannot be described as one thing or the other, as due to either nature or nurture. Rather, they say, every instance of behaviour has to be seen as the
product of a continuing interaction between the components of heredity (nowadays known as genes) and the environmental conditions of development. This means that we cannot simply factor out human behaviour, or for that matter the behaviour of any other creature, into its innate and acquired components. Consider, for example, the work of the beaver. In his paper on The Superorganic, Kroeber had compared the feats of the beaver, in constructing dams, with those of human builders. His conclusion was that although the beavers dam may be as impressive as many a human construction, the beaver and the human achieve their results by fundamentally different means: the former by instinct, the latter by learning. Who would be so rash, Kroeber asked rhetorically, as to affirm that one generation or a hundred or ten thousand of example and instruction would in the least convert the beaver from what he is into a carpenter or a bricklayer or, allowing for his physical deficiency in the lack of hands, into a planning engineer? 25 Some fifty years later, in a paper published in 1964 entitled The impact of the concept of culture on the concept of man, 26 Clifford Geertz returned to the beaver/human comparison. But there was a significant difference. For Geertz recognises that the beavers behaviour is not determined by nature rather than nurture, but is rather the product of an interaction between the two. Accordingly, I take Geertzs paper as representative of the third phase in the history of anthropological thinking about the biology/culture interface: what I call the interactionist phase. Let me quote the relevant passage: Beavers build dams, birds build nests, bees locate food, baboons organise social groups, and mice mate on the basis of forms of learning that rest predominantly on the instructions encoded in their genes and evoked by appropriate patterns of external stimuli: physical keys inserted into organic locks. But men build dams and shelters, locate food, organise their social groups or find sexual partners under the guidance of instructions encoded in flow charts and blueprints, hunting lore, moral systems and aesthetic judgements: conceptual structures moulding formless talents. 27 Thus beavers learn to build dams and humans learn to build shelters. But the form of learning in each case is significantly different. In the case of the beaver, learning consists in the way in which given, genetically prescribed potentials are brought out, within the lifetime of the individual, by appropriate environmental stimuli. What the beaver inherits, with its genes, is not dam-building behaviour but a programme of instructions for the development of dambuilding, which nevertheless depends for its realisation on specific environmental conditions. Human beings, by contrast, do not inherit in the genes a programme for the development of house building. Rather, they inherit a capacity to acquire such programmes. To put it another way, the programme for the development of the human organism in its environment is genetically underdetermined. It has to be completed through the acquisition of additional instructions. And these instructions are encoded in what is commonly called culture, a body of information that is transmitted across the generations by non-genetic means. In short, for human beings there is not just one
channel of inheritance but two. There is the genetic channel, shared with other animals such as the beaver. But there is also a separate, cultural channel. And human behaviour has to be understood as the result of a three-way interaction between both culturally and genetically transmitted information and the environment. 28 Advocates of the interactionist view often claim that they have long since dispensed with the dichotomy between nature and nurture, or between the innate and the acquired. But in fact they have not. The dichotomy is still there, but has simply gone underground. Instead of dividing overt behaviours into those that are innate (such as the smile) and those that are acquired (such as the handshake), the division is made on the level of underlying instructions between innate and acquired components of the programmes that guide all behaviour. The behaviour itself is understood as the consequence of an ongoing interaction between the two, under given environmental circumstances. Towards a relational approach I am not myself content with this way of thinking. I do not believe it makes any more sense to reduce biology to genes than it does to reduce culture to analogous units of information (memes) that inhabit the mind. For in reality, what people do is not merely the effect of genetic, cultural and environmental causes. Genes and culture do not interact with the environment, nor are people and their behaviour the products of such interaction. If we ask what interacts with the environment, the answer is the people themselves. And through such interaction, people actively intervene in shaping the conditions of future development, both for themselves and for others. That is to say, people are the producers as much as the products of their own history, in a continuous process of social life. Let me return for a moment to Clifford Geertz. One of the most significant facts about us, he writes, in the same paper to which I referred earlier, may finally be that we all begin with the natural equipment to live a thousand kinds of life but end in the end having lived only one. 29 Human life, in this view, is conceived as a movement from the universal to the particular, or from biology to culture, entailing a gradual filling up of capacities and closing down of possibilities. I can only conclude that such a view is fundamentally mistaken. The fact is that our bodily equipment, if we can call it that, is not ready-made but undergoes continual formation in the course of our lives. Even the skeleton, for example, grows in a body that is actively doing things, and its precise form is liable to bear the mark of these activities. And the growth of the body is an aspect of the very same developmental process by which we gain proficiency in the particular kind of life that we lead. So what do we begin with? What is already in place at the moment of inauguration of a new human life-cycle? The answer is not just a set of genes but a whole system of relations comprised by the presence of the fertilised egg with its complement of DNA, in a womb, in the body of a mother-to-be, who is in turn alive and active within a particular environment. In short, what each of us begins with is a developmental system. 30 Human beings, then, are not born biologically or psychologically identical, prior to their differentiation by culture. There has to be something wrong with any explanatory
scheme that needs to base itself upon the manifestly ludicrous claim in the words of the evolutionary psychologists John Tooby and Leda Cosmides that infants are everywhere the same. 31 Even parents of identical twins know this to be untrue! The source of the difficulty lies in the notion that culture is an extra ingredient that has to be added in so as to complete the human being. In reality, all those specific abilities that have classically been attributed to culture to walk in a certain way, to speak a certain language, to sit or squat, and so on are incorporated, through processes of development, as properties of human organisms. In that sense, they are fully biological. But and this is the really crucial point biological differences are not genetic. In themselves, genes make no difference. They only make a difference in the context of the life histories of whole human beings, indissolubly body and mind, growing up and, in turn, raising their successors, in a particular environment. 32 Clearly we have a major problem with biology when it comes to human beings. At the root of the problem is our obsession with the idea that for every individual human being there must be something fixed and stable, which is present right from the moment of conception and that remains unchanged for the entire duration of the life cycle. Regardless of what happens to the individual in question, and of what he or she does, it is always supposed to be there. Most often, when people in modern western societies speak of human biology, they do not mean the scientific study of human organisms; they mean this constant thing that is supposed to reside inside each one of us, somehow orchestrating our growth and development. Much of our fascination with genes lies in our understanding that they do indeed remain (virtually) fixed and unchanging for every individual throughout life. Thus they seem to provide concrete proof of the existence of the individual human essence that we had always imagined. No wonder, then, that we jump to the conclusion that our biology must lie in the genes, and therefore that it is the genes that make us what we are. When, some years ago, scientists claimed finally to have unravelled the human genome, we were all told on television and radio, and in the newspapers, that we were witnessing the birth of a totally new era in human understanding, on a par with the discovery of fire or the invention of the wheel. Presidents and heads of state literally queued up to pile on the rhetoric. Pundits proclaimed that our conception of ourselves, as human beings, would never be the same again. But within a few months all that was water under the bridge. For it soon turned out that the number of genes was simply too small to specify much of what makes a human being, and that most of these genes are anyway shared by all kinds of other creatures that could hardly be more different from ourselves, ranging from the mouse to the nematode worm. Now, the scientists proclaimed, they had made a new and even more radical discovery. Contrary to what had previously been thought, the genes do not make us what we are. Instead, we were told, the environment plays a decisive role in shaping human nature. How depressingly familiar all of this sounds! Far from ushering in a radically new conception of ourselves, contemporary science has been rehearsing a nature-nurture debate that has been around, in one form or another, for centuries. The much vaunted human genome project, for example, rests on a central idea, namely that there is such a thing as a human genome in other words, that a context-independent, hereditary specification of the essential form of humanity actually exists. This idea was well
established long before science in a recognisably modern form ever got off the ground. If it continues to dominate our thinking about the advance of human selfunderstanding, it is not because it represents the peak of scientific achievement, but because it is deeply embedded in the institution of science itself. So long as it persists, moreover so long, that is, that the notion of genetic inheritance is wedded to an essentialist definition of the human sub-species the spectre of race will not go away. My argument has been that in order to exorcise the spectre we need to wrest biology away from the stranglehold of geneticism, and to adopt instead a relational approach that focuses on the emergent and dynamic properties of developmental systems. To do so, we must acknowledge that our humanity is not naturally given as a hereditary endowment but is an ongoing historical project or rather, a whole ensemble of such projects that we have to work at. And we have to recognise that every one of us is forged in our organic being within this ensemble and plays his or her part in moving it along. Indeed behind the scenes, away from the razzmatazz of media hype and billion dollar research contracts, a number of biologists, anthropologists and philosophers have been laying the foundations for just such an approach. 33 This is work that is actually set to revolutionise the way we think about ourselves, and I am optimistic that it will eventually prevail. Only then, however, can the spectre of race finally be laid to rest.
Paper presented at the symposium What is special about the gene?, Cardiff University, 11th September 2007 2 Department of Anthropology, University of Aberdeen, UK, tim.ingold@abdn.ac.uk 3 See, for example, P. Descola & G. Palsson eds. 1996. Nature and Society: Anthropological Perspectives. London: Routledge; T. Ingold. 2000. The Perception of the Environment: Essays on Livelihood, Dwelling and Skill. London: Routledge; K. Milton. 2002. Loving Nature: Towards an Ecology of Emotion. London: Routledge; A. Roepstorff, N. Bubandt & Kalevi Kull eds. 2003. Imagining Nature: Practices of Cosmology and Identity. Aarhus: Aarhus University Press. 4 For an authoritative treatment of this history, see G. W. Stocking. 1968. Race, Culture and Evolution. New York: Free Press. 5 A recent discussion of these issues is P. Wade. 2002. Race, Nature and Culture: An Anthropological Approach. London: Pluto Press. In addition, the journal American Ethnologist recently carried a forum discussion on the theme of genomics and racialization (American Ethnologist 2007; 34(2): pp. 210251). 6 See P. M. Graves-Brown. The Ghost of Cain? Neanderthals, Racism and Speciesism. Antiquity 1996; 70: 978-981. 7 See G. W. Stocking. 1968. Race, Culture and Evolution. New York: Free Press, pp. 265-6; T. Ingold. 1986. Evolution and Social Life. Cambridge: Cambridge University Press, pp. 54-55, 381 fn. 14. 8 Modern anthropologys concept of culture has, of course, been subjected to extensive critique over the last two decades. It is debateable how many sociocultural anthropologists would still subscribe to the view that humanity comprises a mosaic of distinct cultures. However the contemporary critique of modernism has tended to exacerbate the split between the biological and sociocultural divisions of anthropology. By and large, the few sociocultural anthropologists who continue to seek a rapprochement with biological approaches in the discipline remain committed to the modernist paradigm, as do biological anthropologists themselves. This commitment is commonly defended in the name of Science, against what is (rightly or wrongly) perceived as a militantly anti-scientific, postmodern humanism. It is no surprise, then, that the post-modern critique of the culture concept has so far had little purchase on anthropological endeavours to reintegrate biology and culture. In the context of these endeavours, culture is still taken to mean much the same as what it meant to the anthropology of fifty years ago. _____________ Genomics, Society and Policy, Vol.4, No.1 (2008) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com 35

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E. Wolf. Perilous Ideas: Race, Culture, People. Current Anthropology 1994; 35(1): 1-12, p.1. Ibid., p. 4. 11 On the misapplication of intelligence testing regimes in cross-cultural contexts, see M. Cole. 1996. Cultural Psychology: A Once and Future Discipline. Cambridge, Mass.: Harvard University Press (Belknap), pp.52-7. 12 Among the most notorious of recent examples was R. Herrnstein and C. Murray. 1994. The Bell Curve: Intelligence and Class Structure in American Life. New York: Free Press. 13 F. Boas. 1940. Race, Language, and Culture. New York: Free Press, p. 165. 14 American Association of Physical Anthropologists. AAPA Statement on Biological Aspects of Race. American Journal of Physical Anthropology 1996; 101: 569-70; also available at http://www.physanth.org/positions/race.html. 15 See T. Ingold. An Anthropologist Looks at Biology. Man (N.S.) 1990; 25: 208-29, pp. 217-18. 16 That is why, when biologists do speak of collectivities of one kind or another, they commonly have resort to the notion of population. The population is understood as an aggregate of discrete individuals, rather than as a group per se. 17 On the debate in American anthropology between those who saw culture as a property of individuals and those who saw it as a property of groups, see Ingold, op. cit., note 7, pp. 230-6. The principal protagonists were Franz Boas on the former side, and Alfred Kroeber on the latter. 18 On the origin of this distinction and its impact on the history of twentieth-century biology, see G. Gudding. The Phenotype/Genotype Distinction and the Disappearance of the Body. Journal of the History of Ideas 1996; 57(3): 525-45. 19 See R. Dawkins. 1976. The Selfish Gene. Oxford: Oxford University Press. The novelty of Dawkinss idea has been hugely exaggerated. Similar proposals have been made, on and off, for decades (these are reviewed in Ingold, op. cit., note 7, pp. 362-4). Outside the realms of advertising, perhaps the best evidence for the idea of the meme as a cultural replicator lies in the success with which the idea itself has caught on (see A. Costall. The meme meme. Cultural Dynamics 1991; 4(3): 321-335). It has not, however, had much success in anthropology, least of all among social and cultural anthropologists, most of whom find the idea repellent. Biological anthropologists have given it somewhat greater credence (see, for example, R. Aunger. 2002. The Electric Meme: A New Theory of How We Think and Communicate. New York: Free Press). It is undoubtedly among cognitive psychologists, however, that it has been most positively received (see S.J. Blackmore. 1999. The Meme Machine. Oxford: Oxford University Press). 20 See E.B. Tylor. 1871. Primitive Culture (2 vols.). London: John Murray; C. Darwin 1874. The Descent of Man and Selection in Relation to Sex (2nd edition). London: John Murray. On the differences between Tylor and Darwin concerning the educability of savages, and Tylors change of heart, see Ingold, op. cit., note 7, pp. 57-8. It is shocking to find that at late as 1972, one of the leading biologists of the day, C.D. Darlington, could still argue in a lecture published by a prestigious academic press that the ranking of classes in modern societies corresponds to hereditary differences in intellectual ability and should be preserved in the interests of civilisation. See C.D. Darlington. 1972. Race, Class and Culture, in J.W.S. Pringle (ed.) Biology and the Human Sciences. Oxford: Clarendon Press. 21 A.L. Kroeber. The Superorganic. American Anthropologist 1917; 19: 163-213. 22 ibid., p. 179. 23 Geertz refers to it by the notion of consensus gentium. See C. Geertz 1973. The Interpretation of Cultures. New York: Basic Books, pp. 37-43. 24 F. Galton. 1874. English Men of Science: Their Nature and Nurture. London: Macmillan. 25 Kroeber, op. cit., note 21, p. 176. 26 The paper is reprinted as Chapter 2 of Geertz, op. cit., note 23. 27 ibid.: pp. 49-50. 28 This is the foundation for the so-called dual inheritance model of gene-culture co-evolution. See P. J. Richerson & R. Boyd. A Dual Inheritance Model of Human Evolutionary Process, I: Basic Postulates and a Simple Model. Journal of Social and Biological Structures 1978; 1: 127-54; C.J. Lumsden & E.O. Wilson. 1981. Genes, Mind, and Culture. Cambridge, Mass.: Harvard University Press; W.H. Durham. 1991. Coevolution: Genes, Culture and Human Diversity. Stanford: Stanford University Press. 29 Geertz, op. cit., note 23, p. 45.
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On the concept of the developmental system, see S. Oyama. 1985. The Ontogeny of Information: Developmental Systems and their Evolution. Cambridge: Cambridge University Press. On the application of the concept within anthropology, see T. Ingold 2000. From Complementarity to Obviation: On Dissolving the Boundaries Between Social and Biological Anthropology, Archaeology and Psychology, in S. Oyama, P.E. Griffiths & R.D. Gray (eds.) Cycles of Contingency: Developmental Systems and Evolution. Cambridge, Mass: MIT Press, pp. 255-279. 31 J. Tooby & L. Cosmides. 1992. The Psychological Foundations of Culture. In J.H. Barkow, L. Cosmides and J. Tooby (eds.) The Adapted Mind: Evolutionary Psychology and the Generation of Culture. New York: Oxford University Press, p. 33. 32 T. Ingold. 2000. Evolving skills. In H. Rose & S Rose (eds.) Alas Poor Darwin: Arguments Against Evolutionary Psychology. London: Jonathan Cape, New York: Random House, pp. 225-246. 33 It would be more accurate, perhaps, to say that a number of approaches are currently being pursued, which have in common a concern to rebalance the relation between evolutionary and developmental processes, away from the strict subordination of the latter to the former that is characteristic of contemporary neo-Darwinism. The approach with which I am most familiar, and to which I have myself contributed, is that of the developmental systems theory (DST) of Susan Oyama and her colleagues. For a representative sample of work in DST across a wide interdisciplinary field including evolutionary and developmental biology, ethology and ecology, psychology, anthropology and philosophy see S. Oyama, P.E. Griffiths & R.D. Gray, eds. 2000. Cycles of Contingency: Developmental Systems and Evolution. Cambridge, Mass: MIT Press. For other approaches, see, inter alia, M-W. Ho & P.T. Saunders, eds. 1984. Beyond Neo-Darwinism: Introduction to the New Evolutionary Paradigm. London: Academic Press; B.C. Goodwin, A. Sibatani & G.C. Webster, eds. 1989. Dynamic Structures in Biology. Edinburgh: Edinburgh University Press; S.A. Kauffman. 1993. The Origins of Order: Self-Organization and Selection in Evolution. Oxford: Oxford University Press; H. Maturana and F. Varela 1973. Autopoiesis and Cognition: The Realization of the Living, eds. R. S. Cohen and M. W. Wartofsky. Dordrecht: D. Reidel; S.B. Carroll. 2005. Endless Forms Most Beautiful: The New Science of Evo Devo and the Making of the Animal Kingdom. New York: Norton; E. Jablonka & M. J. Lamb. 2005. Evolution in Four Dimensions: Genetic, Epigenetic, Behavioral, and Symbolic Variation in the History of Life. Cambridge, Mass: MIT Press.
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The Meanings of the Gene and the Future of the Phenotype

LENNY MOSS 1 Introduction Grasping at Complexity How does one analyze a living organism? Its not as easily settled a question as it may sometimes appear. For all the indisputable success of reductionist approaches in biology we are still not yet so very close to being able to explain how an embryo develops or even how a single cell functions. If biologists were able to build a living organism, even the simplest of living cells, out of purified parts, it would certainly do much to settle methodological and epistemological conundrums over questions of relative holism versus relative reductionism and presumably it would bring biology into a more seamless continuum with the physical sciences. Good intentions and boastful ambitions notwithstanding, we still cannot predict when that feat will be accomplished. And unless and until it is accomplished (and maybe even after that) the study of the living will be uniquely burdened with the dilemma of whether to try to grab onto basic units or parts, hypothetical or otherwise, and then proceed to work ones way up to the complexity of a whole living system, or to begin at some minimum level of intact living complexity and attempt to poke it and probe it, hypothesize about it and take its measure in every conceivable fashion while yet preserving its integrity as a living system. Not that these need be mutually exclusive approaches far from it. But how to relate the one to the other also remains an open question bold claims by behavioural geneticists notwithstanding. Earlier in the century, Niels Bohr famously speculated that there was no way to bridge these two standpoints, that rather, on the model of the wave and particle in quantum mechanics, they would be destined to co-exist independently, in a relation of perpetual complementarity. A protg of Bohr, Max Delbrck, became a pioneer in structuring the physio-chemical investigation of life by way of an informationtheoretic outlook albeit with an on-going expectation that he would eventually hit up against the limits or paradox that Bohr prophesized, 2 which could well lead to the realization of new basic laws of physics. Inspired by Delbrck, Erwin Schrdinger 3 proceeded to predelineate a new informational/linguistic vision of life with his anticipation of an aperiodic crystal that would be the substrate of his so-called hereditary code-script. For Schrdinger however, unlike Delbrck, the reduction of living complexity to bio-molecular information wasnt a strategy for recovering the truth of Bohrs complementarity at a more analytically refined level but rather was the entry-point into the promised land itself. 4 Schrdingers artful rhetoric did much to shape the terminological linguistic, and thereby conceptual, space in which the Watson and Crick breakthrough was received a decade later. Schrdingers own point of departure, however, already presupposed a preformationistic understanding of the relationship of the genotype to the phenotype that he, somewhat naively, took to be the standing view of the genetics of his time.
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In addition to purely epistemological complexities (as if these werent already hard enough), the understanding of the nature of the living organism is far too closely linked to questions of human self-understanding, an irreducibly normative affair, to be able to stand outside of the worlds of social and political interest. In other work Ive suggested that the late nineteenth/early-twentieth century (re)turn to a preformationistic outlook in biology cannot be separated from the hardening and physicalization of social understanding expressed for example in the rising emphasis on race and racialized theories of history, along the contemporaneous formation of a eugenicist social agenda. 5 I will return to the question of the significance of biological formulations for anthropological self-understanding at the end of the paper. The concept of the gene ultimately has to be understood as arising in both epistemological and sociopolitical contexts, although I will only be able to focus on the former in this instant. A concept of the gene, no matter its particular formulation, is put forth as a possible handle with which to grasp hold of the complexity of the organism. Of course many issues turn on just how the nature of that grasp is construed. Both Weismann in Germany, and E. B. Wilson in the U.S., 6 anticipated a gene-like concept prior to the turn of the century. There can be little doubt that by the end of the nineteenth century the time was ripe for something like a gene-concept to emerge. What Mendels paper, rediscovered in 1900, provided was not merely another gene-type concept but a way to put a gene-type concept to work. Whether Mendel himself had conceived of his unit-characters as the basis of a thoroughgoing analysis of the organism or merely as a practical device for aiding plant breeders, as Rafael Falk 7 has argued, has been a subject of debate. Mendels unitcharacter clearly opened a window onto something, but the nature and scope of that something was by no means defined or circumscribed by Mendels findings. Mendel himself did not even distinguish between that which is transmitted in the seed and the traits, like red or white flowers, that eventually come to be seen. By simply referring to the transmission of unit-characters, as if it these were the traits themselves, eg, the red and white flowers, that were transmitted in the seed he spoke in the idiom of preformationism. But if indeed Mendels intent was purely instrumental (as Falk as argued), there was no reason for him to do otherwise as it would merely have been a methodological shorthand. Johanssens (non-preformationist) Gene The distinction between a genotype and a phenotypebetween that which is physically transmitted in the germ and that which comes to appear with maturation in the next generationwas introduced by the Dutch botanist Wilhelm Johanssen who, in 1909, simultaneously introduced the term gene. Johanssen distinguished between the genotype and the phenotype precisely to ward off the temptations of nave preformationism, a fallacy that Johanssen never attempted to hide his disdain for. By distinguishing between a genotype and a phenotype, Johanssen laid the groundwork for genetics to become a modern, independent and basic empirical science concerned with elucidating the relationship between that which is chemically transmitted from one generation to the next and the contextually conditioned realization of a particular organismic outcome from within a certain genotypically prescribed possibility space termed the norms of reaction. 8 Genotype, environment and phenotype thus always constituted a triadic relationship for Johanssen. Notably, it
was this bit of conceptual housekeeping that quite likely induced T.H. Morgan, the embryologist and Mendelian skeptic, to convert to genetics and become the leader of the new discipline. 9 If Johanssens phenotype/genotype distinction provided some conceptual leverage against encroachments of nave preformationism, the exact nature and scope of the relationship of genotype to phenotype remained open and undecided. By 1923 it was clear to Johanssen, for example, that the phenotype cannot be fully decomposed down to an ensemble of separable units but rather that there was a core great central something as he says, which could not and would not be decomposed. Lets take a look at what he had to say: Certainly by far the most comprehensive and most decisive part of the whole genotype does not seem to be able to segregate in units; and as yet we are mostly operating with characters, which are rather superficial in comparison with the fundamental Specific or Generic nature of the organism. This holds good even in those frequent cases where the characters in question may have the greatest importance for the welfare or economic value of the individuals. We are very far from the ideal of enthusiastic Mendelians, viz. the possibility of dissolving genotypes into relatively small units, be they called genes, allelomorphs, factors, or something else. Personally I believe in a great central something as yet not divisible into separate factors. The pomace-flies in Morgans splendid experiments continue to be pomace flies even if they lose all good genes necessary for a normal fly-life, or if they be possessed with all the bad genes, detrimental to the welfare of this little friend of the geneticist. When we regard Mendelian pairs, Aa, Bb and so on, it is in most cases a normal reaction (character) that is the allele to an abnormal. Yellow ripe peas is normal, the green is an expression for imperfect ripeness as can easily be proven experimentally, e.g., by etherization The rich material from the American Drosophiliaresearches of Morgans school has supplied many cases of multiple allelismsmost of all of them being different abnormalities compared with the characters of the normal wild fly To my mind the main question in regard to these units is this: Are experimentally demonstrated units anything more than expressions for local deviations from the original (normal) constitutional state in the chromosomes? Is the whole of Mendelism perhaps nothing but an establishment of very many chromosomal irregularities, disturbances or diseases of enormously practical and theoretical importance but without deeper value for an understanding of the normal constitution of natural biotypes? 10 Now if Johanssen were right, it would not have thereby denied genetics the status of being scientifically or medically interesting and worthwhile but it should have set certain limits upon what Mendelian genetics was in the business of disclosing, that is, what it could be right about. If Johanssen were right, for example, then genetics
would still be providing a certain kind of grasp-hold onto the complexity of the organism, but limited perhaps to certain relatively superficial aspects of it. If Johanssen were right then the truth of genetics would not be that of the wholesale genetic decomposability of the organism qua phenotypeand thus other ways of grasping onto that central core something would still be ultimately required. One may want to surmise that Johanssen, writing thirty years before Watson and Crick, was expressing what is simply become an outdated view; but one would be mistaken. Rather, what will be argued is that precisely on the basis of the best contemporary understanding can we most fully appreciate just how prescient Johanssens insights really were. Johanssen, of course, could not possibly have foreseen the breakthroughs that molecular biology has provided for grasping onto the inner-workings of the organism and yet there is one current meaning of the gene consonant with what Johanssen articulated that continues to stand up to critical scrutiny. My interest in this matter is not particularly historical but rather pertains to how we now should best understand the relationship of genes to phenotypes. Invoking Johanssens perspective is meant to serve as a kind of cognitive/perspectival resource. I will argue that on the basis of strictly current scientific and clinical usage that there are two distinctly different senses of the gene, that each discloses something about the phenotype, but that, properly understood, neither suggests that the phenotype can be decomposed down to an ensemble of genes indeed quite the contrary. I will also suggest that much of the hyperbolic talk about gene as program, blueprints, and the like which has been very successful in finding its way to the public ear, is the result of an illicit conflation of these two meanings. I will then go on to consider some of the implications for our understanding of the phenotype that are derived from these gene concepts taken separately. Finally I will suggest that we are at the threshold of a new transformation in our understanding of the phenotype, and I will make some gestures in the direction of what the consequences this may hold for our theory of evolution and for our anthropological self-understanding. Gene-P versus Gene-D So what is this distinction? And what are these two gene concepts? When one speaks of a gene for blue eyes, or for cystic fibrosis, the gene for breast cancer, or for Marfan Syndrome, one is using a concept of a gene that is defined and specified by its relationship to a phenotype. I call this sense of the gene, Gene-P. What allows something to satisfy the conditions of being a Gene-P is some predictable relationship to the appearance of a certain phenotype. While defined by a predictable relationship to a phenotype, Gene-P, by contrast, is indeterminate with respect to DNA structure, that is, with regard to specific nucleic acid sequence. The P in Gene-P stands for preformationist. To speak as if the transmission of a gene were tantamount to the transmission of a phenotypic trait is to speak in the idiom of preformationism. Preformationism, a child of the seventeenth century, taken to its extreme would hold that all of the traits of the mature organism are already determined and present at birth. The proper contemporary use of Gene-P, however, is not an expression of the ontology of preformationism but only of an instrumental deployment of it. To speak of a Gene-P for a phenotype is to speak as if, but only as if, there were a definite certain something that was transmitted between generations and that dictated a
distinct phenotypic outcome. But as weve already said, Gene-P is indeterminate with respect to its physical referent. It is indeterminate with respect to its DNA sequences and so there is not a certain something that is being transmitted, but rather an uncertain something. How can this be? Would it not simply be a matter of empirically fleshing out what the structure of the physical referent would be? The answer is no. And the reason the answer is no is that what one almost always, if not always, finds in cases of Gene-P, is that it is not the presence of some specific sequence that correlates with the appearance of a phenotype, but rather the absence of some normal sequence resource that is at issue, and there are always many ways for something to be absent. There are, for example, over 900 different documented DNA sequences that may show up as the gene for cystic fibrosis. Likewise, the assurance that two blue-eyed parents may be given that a child of theirs would also have light-colored eyes is based upon the assumption that neither blue-eyed parent has the genetic resource for producing brown-eye pigment, however it is that they may be lacking it. What is inherited, what is passed on, is the lack of something, the lack of a normal resource for producing brown eye pigment. To heritably lack the wherewithal for producing brown-eyes is thereby to possess the Gene-P for blue eyes. As Johanssen suggested, Genes-P can be of great medical and or economic significance but they are essentially, allelic abnormalities that do not provide the basis for decomposing the core of an organism. The genes of classical genetics were Genes-P, but Gene-P is no longer limited to classical methods. The disciplinary context in which the meaning of the gene as GeneP is the most clear-cut is the medical genetics clinic. In the medical genetics clinic, Gene-P is used as a predictor of phenotypic outcomes such as the likelihood of having a child with cystic fibrosis or of contracting breast cancer given a family history. In the modern genetics clinic, traditional family pedigrees can be supplemented or even replaced by the use of molecular probes. Molecular probes are targeted to a specific sequence, but because a Gene-P is indeterminate with respect to sequence, because a Gene-P is characteristically based on the absence of some sequence, probes can only probe for particular ways of not having the normal sequence and never fully rule out the possibility of some other way of not having the normal sequence. What genetic probes can do is to survey some set of the relevant ways that a normal sequence may be absent. If there are 900 documented ways for the normal sequence to be absent resulting in a Gene-P for cystic fibrosis, then it would require 900 different probes to exhaust the possibility of there being a Gene-P for cystic fibrosis given current knowledge although in practice this is modified by statistical data pertaining to the frequency of particular mutations in different populations. Whereas Gene-P is associated with, indeed defined by, a phenotype and thus brings the notion of the phenotype into the semantic reference space of the word gene, Gene-D, by contrast, is defined by molecular, ie, DNA, sequence but is indeterminate with respect to phenotype. If some stretch of DNA provides the template out of which a strand of RNA of complementary sequence is produced, then for a biologist, working at the cell and molecular level, this counts as a gene. To count as a Gene-D entails this and nothing about the ability to predict a phenotypic outcome. But why would that be? And again, might it not be the case that the lack of an ability to specify a phenotypic trait on the basis of DNA sequence is just due to a lack of knowledge?
A possible, in-principle explanation for why a DNA sequence does not determine a specific phenotypic trait would be that any particular DNA sequence can in itself only contribute to any number of different, and often even antithetical, phenotypic outcomes and thus can never be adequate to the task of narrowing down, or specifying, which of these would come to be the case. The D in Gene-D stands for developmental resource and is meant to evoke exactly this type of reasoning. Whereas Gene-P does its conceptual work through offering a peformationist standpoint, but only instrumentally and predictively, as the best we can do in the absence of a full-fledged molecular developmental account of an often pathophysiological outcome, Gene-D assumes a causal-explanatory framework which seeks to elucidate exactly that full-fledged molecular-developmental account, but in order to do so must abstain from delegating causal privileges or priorities prior to the achievement of the empirical account itself. Study upon study at the cell and molecular level shows that any particular Gene-D can participate in, and contribute to, a myriad of different, and even antithetical, phenotypic outcomes and cannot in itself determine which phenotypic outcome it will ultimately contribute to. The character of Gene-D, and why it is indeterminate with respect to phenotypic consequences, is best illustrated with the help of an example. My example called NCAM (for the neural cell adhesion molecule) is representative of a very large class of Genes-D called cell adhesion molecules of which more will be said when the lessons or implications of Gene-D are discussed. NCAM is a member of a very large family of homologous genes called the Immunoglobulin Superfamily (IgSF). 11 The IgSF is one of three such families of related genes associated with cell-adhesion functions, the other two being called the cadherins and the integrins. Humans, and other vertebrates, have only one Gene-D for NCAM in their genome (although as diploid organisms we would have two copies of it). But there are multiple ways in which the very same genetic template can be put to very different uses, which is the point of this example. Like the great majority of molecular genes, that is, Genes-D, NCAM is composed of multiple exons which are the modular units that actually contain the template information for synthesizing messenger RNA and thereby protein. The NCAM gene consists of nineteen exon units. 12 In the process of synthesizing an NCAM protein, first an mRNA transcript is produced in the nucleus that contains all 19 of the NCAM exons. But there are no NCAM proteins that contain the products of all 19 exons. The contingent functional specification of the product of a gene begins with the splicing out of certain exons from the RNA transcript a process that is not and cannot be determined by the gene itself. There are many different ways in which cellular context makes all the difference with respect to what the effects of NCAM gene expression are going to be in any situation. The first of these, weve already seen, pertain to which isoform is expressed, which depends upon the complex of proteins that are involved in splicing. Hundreds of different isoforms of NCAM in mammals have been identified. 13 Characterizing the scope of variability of isoforms derived from differential splicing is still in its infancy and will ultimately have much to say about the relationship of genomes to proteomes. As a taste of things to come, the cell-adhesion molecule called DSCAM found in Drosophila, the famous fruit fly, is capable of giving rise to 38,000 different isoforms, a great many of which have been identified at the messenger level. 14 These isoforms are found on the surface
of embryonic retinal cells as they extend outward in the exploratory formation of synaptic connections in the development of the compound eye of the fly. The fact that a single Gene-D can give rise to a greater number of isoforms of a protein than there are genes in the human genome should be quite suggestive as to where post-genomic biology will be heading. But how and why does variation in isoform matter? The different domains of NCAM that are coded for by one or two exons are associated with different biochemical and physiological activities. The NCAM protein is associated with the cell membrane, with most of its length extending outside of the cell where it may come into contact with other cells. How the NCAM is spliced will affect how, and whether, the protein is attached to the cell membrane and also how much of the protein will extend into the interior, ie, the cytoplasmic compartment of the cell. As each of these domains carries its own functional portfolio, variation in the domains expresssed will have direct and indirect ramifications on the phenotype. Of central importance in the developmental physiology of neural tissue is the balance between neural plasticity, ie, the ability to form new synapses versus neural synaptic stabilization. 15 Without the ability to form new synapses, neural development simply could not take place in the embryo but neither could new learning take place in the adult. However, if there is no synaptic stabilization, then stable behavior patterns could not become established, skills and habits could not be learned and acquired, and memories could not be retained. Now even though all of the NCAM proteins come from the same Gene-D, the form they take will make all the difference as to whether they are contributing to the stabilization of synapses, or to synaptic plasticity, and in either case as to what kinds of synapses are being formed. The largest of the NCAM isoforms, those that are designated as 180 KDa in size, contain the domain coded for by exon number eighteen and contribute to synaptic stabilization as that domain interacts with cytoskeletal components within the neuronal cell. Far more dramatic, however, is the consequence of whether or not the product of the fifth exon domain becomes decorated with large negatively charged chains of polysialic acid (PSA). NCAM isoforms lacking the eighteenth exon domain but heavily decorated with polysialic acid predominate through embryonic development. In the brain of the adult rat, polysialylation is found only in regions that continue to undergo structural rearrangement, ie, in regions associated with new learning. For the rat, whose world is principally disclosed through the olfactory sense, unlike that of the visually-dominant human, the olfactory bulb is a hotspot for structural rearrangement. The loss of PSA-NCAM (polysialylated NCAM)a change that is independent of any changes in the Gene-D for NCAM itselfis associated with the loss of neural plasticity. 16 What is true for NCAM is true for Genes-D in general and for other cell adhesion molecule genes in particular. Cell and developmental context will influence not only what structural form of a cell adhesion molecule is realized from a multivalent genetic template but even how any particular isoform will function. In the 2003 volume of the review journal Current Opinion in Cell Biology, in the issue dedicated to the biology of cell adhesion, the Editors summarily observed that In general, the cellular context can greatly influence the adhesive and signaling properties of a given molecule. The same cadherin behaves differently in different cell types; and the same is true for integrins and other adhesive proteins.
What Must be True about Organisms for Genes-P to Exist? If a gene, empirically understood as a piece of cellular chemistry that has the capacity to serve as a template for RNA synthesis, ie, as a Gene-D, does not and cannot determine a phenotypic trait in itself, then how, one may well wonder, can it even be possible for a Gene-P to exist? Is Gene-P a special subset of Gene-D? If not, then what is it that causes the phenotypic outcome that defines Gene-P? What has to be the case about an organism for Genes-P to exist? And what is the relationship between Gene-P and Gene-D? Throughout most of the twentieth century elucidating the genotype had been the central strategy for understanding the phenotype. Following Mendels lead, classical genetics parsed the phenotype into traits precisely according to whether such parsing was serviceable for further elucidating the genotype. Parsing the phenotype according to the rules of Mendelian inheritance gave birth to Gene-P. There was nothing in the experience of classical genetics that warranted the assumption that a phenotype would be fully decomposable into genotypic units and Wilhelm Johanssen, as weve seen, was dead certain that it would not. However, so long as classical genetics could see an open road ahead for further elaboration of the genotype qua Gene-P, and so long as no more powerful approach for understanding the phenotype came on the scene, nothing stood in the way of continued attempts to decompose the organism into so many Genes-P. This enterprise took a new turn with the characterization of DNA as the heritable source of templates for synthesizing protein, and thus the arrival of Gene-D. Despite the de facto independence of Gene-D as an organizing concept in molecular-level biology, the continued primacy, during the last half of the twentieth century, of the genotype as the means for understanding the phenotype had been based largely on the de facto conflation of Gene-D with Gene-P. While the idea that the phenotype could be fully decomposed into a conglomeration of genes, each of which roughly codes for a trait, began with those zealous Mendelians that Johanssen took to task, in the second half of the twentieth century it has been the conflation of Gene-P with Gene-D that has given rise to the idea of the master-molecule, or blueprint, that is specified simultaneously by its nucleic-acid sequence and its phenotypic consequence. It is this conflationary view of the gene, which borrows and blends from two categorically different disciplinary contexts within biology and medicine, that underlies the genecentered conceptions that have been advanced by certain evolutionary biologists and philosophers, certain evolutionary psychologists, and which has been given a broad public exposure by the likes of popularizers such as Richard Dawkins, Daniel Dennett and Steven Pinker as well as large numbers of science journalists. Looking ahead into twenty-first century post-genomic biology, beyond the conflation of Gene-P and Gene-D, the phenotype itself has become poised to take center stage. The sequencing of the human genome and the move to genomics can well be seen as the culmination of an enterprise and the exhaustion of a research strategy. For many Systems Biology has become the research programme, heir apparent. Ironically, perhaps, it is precisely the empirical knowledge gained within the disciplinary context
of Gene-D that allows us to definitively disambiguate and de-conflate Gene-P and Gene-D. Where for a century much of biology has been structured around the attempt to understand the phenotype on the basis of the genotype, with the culmination of this enterprise in genomics and with the disambiguation of Gene-P and Gene-D a new horizon presents itself. Gene-P and Gene-D, considered separately, each opens a window, albeit very different windows, onto the complexity of the phenotype. The analysis of the genotype can longer be taken as a substitute for that theory of the phenotype that we have yet to realize. Unburdened with the shackles of conflation, both Gene-P and Gene-D can provide new points of entry into the construction of a theory of the phenotype. Beyond conflation, we can now ask what is illuminating about Gene-P and about Gene-D? Listening to Gene-P The Case of Marfan Syndrome Examining two very different examples of Genes-P will help to address the questions that Ive posed about the nature of Gene-P, its relationship to Gene-D, and what kind of window onto the phenotype each gene concept provides when no longer conflated with the other. The two Genes-P that I will discuss are the genes for Marfan Syndrome and BRCA1, the gene for breast cancer. Marfan Syndrome is also known as Abraham Lincoln disease. It was first characterized by Antoine Marfane in 1896 in a five-year-old girl possessed of unusually long tapering fingers. Marfan syndrome 17 appears in one in ten thousand individuals worldwide. It displays a cosmopolitian range of distribution, showing no preference with respect to region, nationality, or gender. Marfan syndrome is characterized by a set of traits, the expression of which are highly variable (pleiotropic). Most characteristic of Marfan Syndrome is a tall, thin stature, sometimes athletic. The face tends to be narrow and the palate high. While it isnt known whether Abraham Lincoln was in fact a Marfan, it is from these features that the association with Abraham Lincoln is derived. Like the five-year-old French girl mentioned above, Marfan individuals will frequently have unusually long limbs with long and tapering fingers and toes. Other features include a breastbone that is either pushed in or pushed out, a propensity for scoliosis, joints that are unusually loose and somewhat injury prone, off-center lenses in the eye and myopic vision andthe medically most significant traitis susceptibility to aortic aneurism that can only be detected by an echocardiogram. 18 Marfan Syndrome is a disease of connective tissue. It is the result of a failure to properly incorporate the connective tissue protein fibrillin-1 into the microfibrils of developing connective tissue throughout the body. There are at least 150 mutations of the Fibrillin-1 gene (Gene-D) associated with Marfan Syndrome. 19 Any of these could show-up as a Gene-P for Marfan Syndrome. As is typical of a Gene-P, any of these genes for Marfan Syndrome can be tracked by pedigree analysis or by molecular analysis given the right molecular probes. What makes a gene a gene for MarfanSyndrome, that is, a gene for a certain phenotype and thus a Gene-P, is its predictive relationship to a phenotype. But let us consider just what is the relationship of a gene for Marfan-Syndrome to the phenotype. What is it that causes the characteristics associated with the phenotype? Is there any good sense in which a gene for Marfan Syndrome can be construed as carrying information or coding for a trait? Does the
gene for Marfan Syndrome tell the developing body to be tall and lanky, or to have a high palate or to be near sighted? Certainly not. The features of Marfan Syndrome, like that of blue eyes, are the results of what human bodies do in the absence of a certain otherwise typical molecular resource. The wherewithal for responding to this absence is inherent in the complex systematicity of the phenotype, in its adaptive plasticity, properties that simply cannot be decomposed down to atomic units. The Gene-P for Marfan Syndrome reveals this systematicity, this capacity, given a certain constraint or perturbation, for the developing phenotype to developmentally style itself in a recognizable way. There is no gene that codes for an Abraham Lincoln phenotype, but Marfan Syndrome reveals that the systematic properties of the human phenotype are such that, given a certain class of perturbations, some set of Marfan characteristic will result. Marfan Syndrome is an expression of the polyphenism of the human phenotype, that is, its ability to phenotypically shift directions while yet retaining its overall integration as a functional system. Within a context of family resemblance, Marfan individuals will vary with respect to specifics. Individuals who differ with respect to which of the 150 mutations they carry are seen to show phenotypic differences, yet some individuals with the same mutation will also differ and some individuals with different mutations will present a great deal of resemblance. In addition, a Marfan phenotype may be found in individuals without a mutant fibrillin-1 gene at all, because any perturbation, genetic or otherwise, that interferes with fibrillin synthesis, transport, or microfibril assembly can lead to the same type of polyphenic outcome. Now what about the Gene-D for fibrillin? If the example of Marfan Syndrome has made good on the claim that a Gene-P is indeterminate with respect to molecular structure or sequenceand that it is only an instrumental predictor of the phentotype it is associated withwhat does the Marfan example have to say about the claim that any Gene-D will be indeterminate with respect to phenotype? As is the case in relation to any, or almost any, Gene-P, there is no corresponding normal gene with specificity for a phenotypic contrast class. The Gene-D for fibrillin-1, ie, the normal gene, does not, for example, favor a short and squat phenotype any more than it favors a tall and slender one. The Gene-D for the fibrillin-1 template sequence can be used in many different ways in different contexts and it will always be the larger developmental context that will determine toward which phenotypic outcome the gene-product will contribute. The Case of BRCA1 BRCA1, the gene for breast cancer, provides another useful example because it differs from the gene for Marfan Syndrome in all its particulars and yet the take-home lessons about the relationship between Gene-P and Gene-D, and what it is that a Gene-P reveals about the phenotype, are quite consistent. BRCA1 has been the flagship gene for the enthusiasts of germ-line genetic testing. 20 A positive result with a molecular probe test for the presence of a BRCA1 gene correlates with an 85% likelihood that a woman from a family with a history of breast and/or ovarian cancer will contract breast cancer at some point during her own lifetime. Defined by this phenotypic prediction, BRCA1 or the gene for breast cancer is a Gene-P. As is the case with other Genes-P, there are numerous mutations (at the BRCA1 locus) that meet the criteria for being a gene for breast cancer. Owing to the interest that BRCA1
has garnered since first being identified, the molecular biology of the Gene-D, which alas is also called BRCA1, has been intense since it was first identified over 20 years ago. Unlike fibrillin, which is secreted into intercellular space and becomes a structural component of the bodys connective tissue, BRCA1 (the protein) is active in the nucleus of the cell. The distribution of BRCA1 with respect to tissue type and developmental stage is described as ubiquitous. Just as the Gene-D for fibrillin is not a gene for short and stocky phenotypes, but like any Gene-D is indeterminate with respect to phenotype, the normal BRCA1 is not a gene for healthy breasts, nor does it show any specificity for breasts at all. BRCA1 is a large multi-modular protein that has been implicated in several different functions within the nucleus transcriptional regulation, DNA repair, chromosome remodeling, and the targeting of proteins for intracellular degradation - and it is apt to be found in every cell in every tissue in the body. 21 The tips of the BRCA1 protein have the capacity to bind to the RNA polymerase enzyme, and the middle region of the protein has been shown to bind to a wide variety of both transcriptional enhancers and transcriptional repressors. The interesting question, then, becomes: why do mutant germline forms of BRCA1, while present and active in every type of cell in the body, show up as a Gene-P specifically for breast cancer? 22 What does this Gene-P disclose about the nature of the phenotype (and perhaps about cancer as a potential inherent within the phenotypic possibility space)? The BRCA1 protein in the nucleus of the cell has been shown to serve as a kind of platform upon which other proteins assemble in stage- and tissuecontingent ways. The number of proteins that interact with BRCA1 has been described as astronomical. What becomes suggestive is the possibility that what may best account for why germline mutation in the BRCA1 gene shows up as a Gene-P exclusively for breast cancer can be best approached in terms of the role of the BRCA1 protein in a complex network of interactants. In other words, is the Gene-P for breast cancer giving us a porthole, not onto the decomposability of the phenotype, but onto previously invisible, network-theoretic properties of the phenotype? We will borrow from the scale-free network analysis developed by the physicist Albert-Lszl Barabsi. 23 In studies of the proteome, that is the entire ensemble of expressed proteins, of the single-celled organism yeast, Barabsi and co-workers 24 looked at yeast proteins simply in terms of the number of the other proteins that any particular protein interacted with. It has been typical of Barabsis studies of networks of all kinds, from social networks, airline flight patterns and the Internet, to living cells, to find that most nodal points, usually around 80%, have only small numbers of linkages to other nodes, whereas the remaining 20% are linked to many other nodes and thus constitute the hubs. The diameter of a system, network-wise, can be reckoned in terms of the maximum number of links that it would take to connect any two nodes in the system. Hubs would clearly play a critical role in maintaining a fixed diameter of a system and when, for example, yeast species have evolved the ability to metabolize new substrates, investigators have found that systematic adjustments take place in the metabolic network such as to enable the diameter of the network to remain constant. 25 In further examining yeast, Barabsi and coworkers found that 93% of proteins have five or fewer links, whereas only 7% of proteins have 15 or more links. Not surprisingly, the deletion of only a small percentage of the weakly
linked proteins proved to be lethal to the yeast, whereas the deletion of the majority of the hub proteins proved to be lethal. Although purely speculative at this point, suddenly we have a completely new model for what a Gene-P might be revealing about the phenotype. First of all, for something to show up as a Gene-P, it cannot be a developmental-lethal. If a gene product served as a hub in every tissue, or in any developmentally vital process, its absence would likely be lethal and so not show up as a Gene-P at all. Breast cancers associated with germ line mutations of BRCA1 are quite variable in terms of age of onset, but seldom if ever, occur before puberty and most often occur beyond a womans childbearing age. It could turn out to be the case that BRCA1 isoforms play a sensitive role in maintaining something like a uniform network diameter in the nuclear regulatoryprotein system of post-pubescent mammary cells. Because the post-pubescent mammary gland will constitute its own distinctive biochemical context, it is wholly plausible that an otherwise ubiquitous molecule could play a distinctive role from a network perspective. Should this prove to be the case, then it would simply be a kind of quirk about the systematic relationships of regulatory proteins in the nucleus of mammary cells that would result in BRCA1 mutations showing up as Genes-P for breast cancer, but it would be a quirk that could allow this Gene-P to reveal something hitherto invisible and unimagined, not about the decomposability of the phenotype, but, quite to the contrary, about the systematic, and thus indivisible, properties of the phenotype resident in every nucleus in every cell of the living body. Interrogating Gene-D Finally, what window or windows onto the phenotype might be revealed by Gene-D when no longer burdened by conflation with Gene-P? In a recent article entitle Genes Classical and Genes Developmental: The Different Use of Genes in Evolutionary Syntheses, the developmental biologist, textbook author, and historian of biology Scott Gilbert, 26 writing in a largely pluralistic mood, provides a perspicuous comparison between the beliefs about genes held by the population geneticists who advanced the Evolutionary Modern Synthesis and those of the contemporary molecular biologists who are trying to advance a new evolutionary-developmental, or Evo-Devo, synthesis. Gilbert distinguishes these as Population Genes versus Developmental Genes. I will just pick out some of the more salient features of his comparison. The population genes, whose physical referent were hypothetical, were thought to be atomistic units responsible for distinctively different enzymes and structural proteins that would result in distinctively different phenotypic traits with different fitness values for adult organisms competing for survival. By contrast, the developmental genes, being characterized by molecular biologists interested in evolution have been found to show great similarity, not difference, across taxa; to be associated not with enzymes and structural proteins but with signaling and the regulation of transcription and splicing; to be most significant in their expression not in the adult but in the embryo; and to be context-dependent parts of a pathway rather than acting in a context independent atomistic fashion, as the population geneticists had assumed.
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It should be evident at this point that what Gilbert has described as the presuppositions of population genetics about the nature of the gene are exactly what Ive described as coming to constitute the conflationary view. What Gilbert has described as the developmental gene is exactly what has emerged out of the disciplinary context of Gene-D. 27 But in seeking to clarify the further implications of Gene-D for understanding the phenotype, we can supplement the characterization that Gilbert has provided with a comparative analysis of the findings of different genome projects and other studies that have made evolutionary comparisons from the point of view of Gene-D. After all, the output of genome projects is simply compendia of Genes-D, and one way of asking what Gene-D can tell us about the nature of the phenotype is to see how these compendia change over evolutionary time. 28 Comparative Genomics and Gene-D When we look at organisms of different levels of complexity, single-celled to multicellular, invertebrate to vertebrate, fish to mammal, mouse to human, what kinds of changes in the genomes appear to coincide with changes in the complexity of the organism? The Human Genome Project upset traditional expectations by revealing that humans have only twice as many genes as the fruit fly and only one third more than the tiny nematode worm, C. elegans. 29 Genes-D, as weve already mentioned, are composed of modular units called exons, and it turns out that even this very moderate difference in gene number is based largely on the reshuffling of old exons to produce new combinations, with less than 7% of the increase in gene number based on apparently new modules. So, what we see at the level of genomic differences is that what appears to correlate with changes in complexity is not gross increases in novel genetic resources but rather the intensification of the ability to use the same basic resources in a greater number of ways. What we see at the level of comparative genomics becomes greatly magnified at the level of comparative proteomics. While vertebrates, including humans, have only at most twice as many Genes-D as invertebrates, the complete set of expressed proteins derived from the vertebrate genome appears to be at least five times as great as that derived from the invertebrate genome. The difference between genome size and proteome size would be largely accounted for on the basis of the ability to generate multiple isoforms through differential RNA splicing, as we previously discussed. So, we now know that phenotypes of different levels of complexity are composed of largely the same set of modular resources, but are used in increasingly flexible and nuanced ways. Can the window that Gene-D opens up on the phenotype give us any more insight into how this expansion of the use of genetic modularity is distributed? Is it, for example, evenly distributed across the genome or is it lumpy? And if it is lumpy, does the lumpiness have a meaning that we can interpret? By the looks of some recent studies, the answer to these questions appears to be yes. A systematic comparison 30 between the DNA sequences of human chromosome 19 and those of the homologous chromosomal regions of the mouse suggests that the ensemble of Genes-D that constitute a genome fall into two distinct categories. On the one hand, there are unique, single copy-genes that are dispersed through the genome. On the other hand, there are families of closely related genes that are grouped together on the chromosome in tandem clusters. In comparing the human and mouse
sequences, what was found was an overwhelming conservation of sequence of single-copy genes and extensive differences in genes residing in tandem familial clusters. Given what we have already observed, a little bit of extrapolation would not be out of order. What appears to be the case is that a core set of single-copy genes has been a constant throughout the animal kingdom going back to the most primitive stages. Might it be the case that exactly those genes that provide the templates for basic enzymatic and structural capacities that the population-theoretic architects of the Evolutionary Modern Synthesis assumed would be the basis of evolution, are precisely those that have by and large not evolved at all? The evolutionary history of Genes-D appears to be associated with the expansion and contraction of differentiation of families of closely related genes or gene-families that are found to be present in tandem clusters on chromosomes. Is there any specificity to which gene-families are found to expand in relation to apparent evolutionary increases in organismic complexity? In their 2002 report in Science magazine, J.A. Bailey et al. found that the expansion of gene families comes about through an incomplete duplication of genes, referred to as segmental duplication, that results in the reshuffling of modular exon units and thereby the production of greater protein diversity. 31 They found that such segmental duplication is not distributed randomly throughout the genome. Rather they report that genes associated with immunity and defense, membrane surface interactions, drug detoxification, and growth/development were particularly enriched. While there are doubtlessly interesting things to say about all four of these categories, I will focus briefly on one of which weve already introduced. Cell adhesion molecules constitute an important subset of those gene families associated with cell surface interactions. The Immunoglobulin Superfamily (IgSF), of which I said NCAM is a member, would come under the heading of two of the groups cited above membrane surface interactants and genes associated with immunity and defense. 32 Let us consider what one can construe about the nature of the phenotype through the porthole that the Genes-D of the IgSF provides. Whereas humans have only double or fewer the number of genes overall than the fruit fly or worm, there are 765 IgSF genes in the human genome compared with 140 for fly and 64 for worm. It is estimated that the number of isoforms of proteins from the human IgSF alone would exceed the entire genome size of both fruit fly and nematode worm. All indications are that the comparative findings for other cell adhesion gene families, the cadherins and the integrins, would be quite similar. But what might this tell us about the nature of the evolving phenotype? To answer this question, imagine first that a cell (cell #1) has a single receptor on its surface that is capable of binding to some closely related range of ligands (a ligand simply being a molecule with which a receptor may bind). And let us say that when the receptor binds to the ligand, it can transmit a signal into the cell that results in some change in the physiological and/or transcriptional state of the cell. Now, let us compare this to two other scenarios. In the second scenario (cell #2), let us imagine that for the same range of ligands that our one receptor could bind to, we now have 10 different receptors, each of which specializes in binding some subset of that same range of ligands, and that each of these receptors can then transmit a different signal, thus one of ten different signals, to the interior of the cell. For our third scenario (cell #3), let us imagine that we now
have ten different receptors that vary, not with respect to their binding specificity, but only with respect to the signal that they transmit back to the interior of the cell. Taken together, scenarios two and three (cells #2 & #3) represent a marked increase both in the sensitivity of the cell to nuanced differences in its surround, properties that could also be described as an increased openness of the organism to its environment or its world, and in a measure of increased autonomization, whereby the internal state of the cell can determine which receptors to use to probe its surround, a property that could also be described as increased detachment. 33 Ive been speaking of the cell as if it were a kind of microcosm of the whole organism in its relationship to an environmental surround, but lets also think of it as the unit of multicellular development. A developing organisms developmental trajectory is largely realized through the interaction of its cells with each other and with aspects of their environmental surround, ie, their world. Where an organism is composed of cells that have evolved the capacities of cells #2 & #3 (as opposed to merely that of cell #1) there would be an enhanced capacity for making fine distinctions about their surround, for executing internal-state-dependent choices about how to respond to even the same stimuli, and thus a massively greater capacity for phenotypic flexibility, responsiveness, and adaptability. The evolutionary expansion of the repertoire of cell-surface adhesion and signaling receptors with the IgSF and other gene-superfamilies can be seen as a key factor in the evolution of world-openness and detachment ie, as what we experience as increasingly complex forms of life. Phenotype First? The analysis of Gene-P and Gene-D aspires to provide a perspective with which to break bread once again with Johanssen and rethink the meaning of genes and phenotypes from their roots up. I argued that from at least two different angles we can see why the question of the phenotype is back on the table. What Gene-P and Gene-D both reveal, albeit in different ways, is that there are systematic, self-organizing capabilities of the phenotype which will not yield to the kind of decompositional approach that has held sway during much of the past century, nor for that matter any gene-centered approach at all. Without even attempting to survey exhaustively the relevant sources, I will mention a few of the more salient examples. In the Millennium Issue of the prestigious molecular biology journal Cell, Marc Kirshner and Tim Mitchison of Harvard and John Gerhart of Berkeley, 34 criticize the limits of the machine metaphor in biology, and describe their postgenomic proposal for an integrated cell and organismal physiology, somewhat light-heartedly, as molecular vitalism. What is not light-hearted for them is the idea that the phenotype needs to be understood on its own terms, and structured neither on the basis of the machine metaphor nor that of genetic information. In their more recent The Plausibility of Life, Kirschner and Gerhart 35 draw on the latest findings in cell and developmental biology to explain the active role of organisms (ie, of phenotypes) in facilitating the production of evolutionary variation. In their anthology Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology, theoretical biologists Gerd Mller and
Stuart Newman, 36 along with contributors to their volume, have been exploring the idea that organismal form originates with the inherent properties of living tissues, ie, of the phenotype, and that genes are secondary factors whose role began largely as that of stabilization. Likewise, contributors to the recent anthology called Cycles of Contingency 37 share the inclination to recontextualize genes, understood in a Gene-D kind of way, as one resource among many, in conceptualizing the dynamics of developmental systems. The most sustained and impressive effort of all, however, has been that undertaken by biologist Mary Jane West-Eberhard, 38 whose 800 page tome is entitled Developmental Plasticity and Evolution. West-Eberhards goal is nothing less than a radical transformation of our theory of evolution based upon a phenotypecentered biology. Much of West-Eberhards painstaking study is devoted to documenting the ubiquity of polyphenisms across all living taxa. A polyphenism is the ability of an organism to undergo radical shifts in its phenotypic expression. This often involves shifts in developmental timing that can have drastic effects on the phenotype including the entire loss of a later stage of development. Of the 113 species of salamander, for example, that undergo metamorphosis, 37% of these species are found to have adults that do not always undergo metamorphosis. The loss of a later stage of development is known as neoteny, and it has played a major role in various evolutionary events and transitions (including human evolution as discussed below). Polyphenism may be a source of both de novo evolutionary innovation or the redeployment of phenotypic forms already present within a latent developmental and/or ecological phenotyperesponse repertoire. There are, for example, 27 genera of fish with facultative airbreathing capabilities. The colonization of land was achieved in her view, first of all, not through the evolution of a new species, but rather by way of polyphenic adaptations by a species already invested with facultative air-breathing capability. The capacity for breathing on land was already anticipated and multiple times, by genera of fish most of whom did not give rise to land inhabiting species. The systematic capability of the phenotype to undergo adaptively plastic transformations in response to a new input, in West-Eberhards model, constitutes the principal source of evolutionary innovation, thus shifting much of the adaptive and innovative centre of gravity back to the systematic capacities of the organism itself. She suggests a four-stage model of adaptive evolution in which genes may play two decidedly different roles. These roles, as it happens, correspond well to my GeneP/Gene-D distinction. These stages are as follows: 1. New Input:The phenotype is exposed to some form of perturbation that could be either environmental or genetic. If genetic it would be in the sense of Gene-P. 2. Phenotypic Accommodation: The organism draws upon its plastic, polyphenic capability to respond adaptively to the challenge. 3. Recurrence or Initial Spread: The phenotypic shift spreads through the population either due to the recurrence of the initial input or the spread or other means of inducing the phenotypic shift. To this I would add the suggestion that the phenotype-illiciting input could become stabilized as part of the organisms constructed niche, which in the case of humans means cultural institutionalization.
4. Genetic Accommodation: Unlike the initial input, which could be a single mutation or an environmental cue, that triggers the phenotypic shift, genetic accommodation takes places at multiple loci (this would now be the Gene-D sense of genetic). Genetic Accommodation occurs simply by way of natural selection (i.e., differential survival) occurring within the context of the new selective regime introduced by the phenotype. The genetic heterogeneity is that which was already present in the population prior to the phenotypic shift. Genetic accommodation improves the novel phenotype in three or more different ways. These are: a) adjusting regulation, to change the frequency of expression of the trait or conditions under which it is expressed, b) adjusting the form of the trait, its integration and efficiency, c) reducing disadvantageous side effects. The resonance between West-Eberhards model and my distinction between, and analysis of, Gene-P and Gene-D, shouldnt be too difficult to discern. West-Eberhard thinks that the most likely source of the initial input is environmental, and she may well be right, but she considers a genetic mutation to be a relevant candidate as well. This depiction of a mutation constituting, not new information for the phenotype, but a perturbation to which the phenotype responds in a coherent systematic fashion, is exactly in tune with the characterization of Gene-P, as is the symmetry she depicts between such a mutation and an environmental shift (ie, two types of perturbations) that could trigger the same response. The process of genetic accommodation, as she understands it, entails selection at multiple loci, which is also to say that none of the loci, independently has a determinate relationship to the resulting phenotype. Genetic accommodation, sensu West-Eberhard, is about Gene-D. Perhaps the best way to conceive of the process of genetic accommodation is to recall the clustered groups of related genes associated, for example, with cell-cell recognition and adhesion. How an organism deploys its repertoire of cell-adhesion molecule variants is a problem in the regulation of a complex system. The improvement and stabilization of the new phenotype would be a complex function of many regulatory nodal points. Minute differences in both coding and non-coding regions of DNA could confer relative advantages or disadvantages in a wholly complex and context dependent fashion. Selection may be thought of as akin to that of multiple parallel processing systems that have already been entrained toward realizing that outcome that the adaptive phenotype had established, but are now competing in the ability to best achieve it. With Gene-P, and Gene-D clearly distinguished, and no longer conflated, it is all the more easy to appreciate West-Eberhards proposal that in evolution it is the phenotype that leads the genotype. Developmental Clues and the Origins of the Human Phenotype Beginning with Herder and Kant in the mid-eighteenth century, there arose a philosophical anthropology that located the natural basis for the higher cognitive faculties of humans not merely in a new adaptation but in a full-bodied, systematic breaking awaya loss of organismic specialization, a weakening of the senses, a weakening of the body, a loss of directed skill, a general developmental underdetermination and underdevelopment, and thereby detachment from a stable, tightly coupled, specialized relationship to particular natural surrounds. These early perceptions were given a more firm empirical foundation by the German
philosophical anthropologists of the mid-twentieth century, such as Helmuth Plessner and Arnold Gehlen, who associated these traits with the idea that the hominid line arose by way of neotinization (or juvenalization) from our ape ancestor. German philosophical anthropology, reaching its apex between the wars, suffered a starcrossed fate, failing to succeed in gaining a foothold in the Anglophone philosophical world. The empirical case to be made for the neoteny-based-evolution of the hominid line has only become more compelling over time and has been persuasively represented in a popular book by Clive Bromhall 39 entitled The Eternal Child. The case for neoteny is put forward both by demonstrating the far greater similarity of the adult human with the very young chimp, and by considering the systematic consequences of retarding the rate of maturation at different early stages of development. With the upper body developing prior to that of the lower body, much of the morphological transition associated with the evolution of the upright posture and bipedalism can be accounted for on the basis of extending the growth phase during which legs are formed and lengthened. Similarities with the juvenile chimp but not the adult chimp include the vertical attachment of the head to the spinal column, a small jaw, more flattened face, big rounded skull, the everted lips, the sparseness and pattern of distribution of hair, the low position of nipples, the frontal position of the vulva, the retention of the outer labia and the hymen and the lack of the penis bone. It is interesting to note in this regard that bonobos, who while closely related to chimps, are distinguished from chimps by their female dominant social structure and a polymorphous sexuality that serves as the social glue of an essentially non-violent system of social relation, lie between humans and chimps on the scale of neotinization. As compared with chimps, bonobos have more delicate facial features, more rounded skulls, higher foreheads, higher voices, lighter bones, longer legs, more upright walking, a slower rate of maturation after birth, and the retention of the more frontal position of the vulva that allows bonobos, like humans, but unlike chimps, to mate face to face. Despite stunning evidence for the role of polyphenism in general and neotinization in particular in human evolution, and despite the fact of philosophical intuitions about human detachment and underdevelopment that date back 250 years, late twentieth century thinking about the biology of human psychology, culture and cognition had been almost univocally devoted to piecemeal models of adaptation in which domain specific cognitive modules had been hypostatized very much in the image of conflationary genes taken to another level. In recent years however there has been a coalescence of recognition coming from disparate directions of the essential sociality of the human organism. Neotinization was by no means the entire basis of the evolution of the human socio-cultural capacity but it may well have been a necessary point of departure. Those who have been looking for language and reason in the brain (and the genes that code for them) have been looking for the wrong thing in the wrong place. Language, as Merlin Donald 40 has taught us, didnt evolve in the brain box; it evolved in socio-cultural space. What we need and are beginning to find in the human brain are the bases whereupon humans can be susceptible to each other, and thus participants and co-producers in the ever-changing games of language, with domaingeneral, cross-module executive capacities for leading our own epigenetic formation, interactively, in and through the socio-cultural matrix. In the image of the
new appreciation for the role of group selection in the evolution of sociality, neurologically based advances in social capacity could have been drawn out of the vast hominid phenotypic possibility space and stabilized in socio-cultural ritual that would be selectively advantaged in an environment of inter-group competition. I have begun to explore elsewhere the implications of this work for philosophical anthropology and social theory. 41 Suffice it for now to suggest that the shift to a new phenotype-centered biology will bring with it also opportunities, albeit not inevitabilities, for new and renewed shifts in anthropological self-understanding with all the ethical and socio-political implications that that might entail.
Department of Sociology and Philosophy, University of Exeter, UK Lenny.Moss@exeter.ac.uk see N. Roll-Hansen. The Application of Complementarity to Biology: From Niels Bohr to Max Delbrck. Historical Studies in the Physical and Biological Sciences 2000; 30: 41742; D. McKaughan. The Influence of Niels Bohr on Max Delbruick: Revisiting the Hopes Inspired by Light and Life. Isis 2005; 96: 507-529; A. Domondon. Bringing Physics to Bear on the Phenomenon of Life: The Divergent Positions of Bohr, Delbrck, and Schrdinger. Studies in the History and Philosophy of Biological and Biomedical Sciences 2006; 37: 43388. 3 E. Schrdinger. 1944. What is Life? Cambridge: Cambridge University Press. 4 L. Moss. 2003. What Genes Cant Do. Cambridge MA: MIT Press. 5 L. Moss. 2004. Human Nature, the Genetic Fallacy and the Philosophy of Anthropogesis Jahrbuch 2004 of the Kulturwissenschafliches Institut., ed. Jorn Rusen. 6 J. Maienshein. 1987. Defining Biology: Lectures from the 1890s. Cambridge MA: Harvard University Press. 7 R. Falk. The Dominance of Traits in Genetic Analysis. Journal of the History of Biology 1991; 24: 457-484. 8 W. Johanssen. Some Remarks About Units in Heredity. Hereditas 1923; 4:133-141. 9 R. Falk. The Struggle of Genetics for Independence. Journal of the History of Biology 1995; 28:219246. 10 Johanssen, op. cit. note 8 11 A. Barclay. Membrane proteins with immunoglobulin-like domainsa master superfamily of interaction molecules. Seminars in Immunology 2003; 15: 215-223. 12 G. Povlsen, D. Ditlevsen, V. Berezin & E. Bock. Intracellular Signaling by the Neural Cell Adhesion Molecule. Neurochemical Research 2003; 28: 127-141. 13 A. Zorn & P. Krieg. Developmental Regulation of Alternative Splicing in the mRNA Encoding Xenopus laevis Neural Cell Adhesion Molecule (NCAM). Developmental Biology 1992; 149:197-205. 14 B. Gravely, A. Kaur, D. Gunning, S. Zipursky, L. Rowen & J. Clemens. The organization and evolution of the Dipteran and Hymenopteran Down syndrome cell adhesion molecule (Dscam) genes. RNA 2004; 10: 1499-1506. 15 L. Rnn, B. Hartz & E. Bock. The neural cell adhesion molecule (NCAM) in development and plasticity of the nervous system. Experimental Gerontology 1998; 33:853-864; L. Rnn, V. Berezin & E. Bock.The neural cell adhesion molecule in synaptic plasticity and aging. International Journal of Developmental Neuroscience 2000; 18:193-199. 16 A. Dityatev et al. Polysialylated neural cell adhesion molecule promotes remodeling and formation of hippocampal synapses. Journal of Neurosciences 2004; 24: 9372-9382. 17 V. McKusick. Heritable disorders of connective tissue. III The Marfan Syndrome. Journal of Chronic Diseases 1955; 2:609-644. 18 D. Milewicz, H. Dietz & D. Miller. Treatment of Aortic Disease in Patients with Marfan Syndrome. Circulation 2005; 111:e150-e157. 19 H. Dietz & R. Pyeritz. Mutations in the Human Gene Fibrillin-1 (FBN1) in the Marfan Syndrom and related disorders. Human Molecular Genetics 1995; 4:1799-1809; P. Robinson & M. Godfrey. The molecular genetics of Marfan syndrome and related mircrofibrillopathies Journal of Medical Genetics 2000; 37: 9-25. _____________ 56
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Genomics, Society and Policy, Vol.4, No.1 (2008) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com
J. Paterson. BRCA1: a review of structure and putative functions. Disease Markers 1998; 13: 261274. 21 K. Yoshidia & Y. Miki. Role of BRCA1 and BRCA2 as regulators of DNA repair, transcription, and cell cycle in response to DNA damage Cancer Science 2004; 95: 866-871. 22 B. Billack & A.N.A. Monteiro. BRCA1 in breast and ovarian cancer predisposition. Cancer Letters 2005; 227: 1-7. 23 A-L. Barabsi. 2002. Linked: The New Science of Networks. Cambridge MA: Perseus. 24 H. Jeong, S. Mason & A-L. Barabsi. Lethality and centrality in protein networks. Nature 2001; 411: 41-42. 25 A-L. Barabsi & Z. Oltvai. Network Biology: Understanding the Cells Functional Organization. Nature Reviews Genetics 2004; 5: 101-114. 26 S. Gilbert. 2000. Genes Classical and Genes Developmental: The Different Use of Genes in Evolutionary Syntheses in The Concept of the Gene in Development and Evolution: Historical and Epistemological Perspectives. Beurton, Falk & Rheinberger (Eds). Cambridge: Cambridge University Press. 27 L. Moss. One, Two (Too?), Many Genes. The Quarterly Review of Biology 2003; 78: 57-67. 28 L. Moss. Redundancy, Plasticity, and Detachment: the Implications of Comparative Genomics for Evolutionary Thinking Philosophy of Science 2006; 73: 930-946. 29 Ibid. 30 P. Dehal et al. Human Chromosome 19 and Related Regions in Mouse: Conservation and LineageSpecific Evolution. Science 2001; 293:104-111. 31 J. Baily. Recent Segmental Duplications in the Human Genome. Science 2002; 297:1003-1006. 32 Barclay, op. cit. note 11. 33 Moss, op. cit. note 28; L. Moss. 2008. Detachment, Genomics and the Nature of Being Human. In New Visions of Nature: Complexity and Authenticity, Drenthen, Keulartz, Proctor (Eds), Springer International Library of Environmental, Agricultural and Food Ethics (in press). 34 M. Kirschner, J. Gerhart & T. Mitchison. Molecular Vitalism. Cell 2000; 100:79-88. 35 M. Kirschner & J. Gerhart. 2006. The Plausibility of Life. New Haven: Yale University Press. 36 G. Mller, & S. Newman (Eds). 2003. Origination of Organismal Form. Beyond the Gene in Developmental and Evolutionary Biology. Cambridge MA: The MIT Press. 37 S. Oyama, P. Griffiths & R. Gray. (Eds) 2001. Cycles of Contingency: Developmental Systems and Evolution. Cambridge MA: The MIT Press. 38 M.J. West-Eberhard. 2003. Developmental Plasticity and Evolution. Oxford: Oxford University Press. 39 C. Bromhall. 2003. The Eternal Child: Has Evolution has Made Children of Us All. London: Ebury Press. 40 M. Donald. 2001. A Mind So Rare: The Evolution of Human Consciousness. New York: Norton & Company. 41 L. Moss. Contra Habermas and Towards a Critical Theory of Human Nature and the Question of Genetic Enhancement. New Formations 2007; 60: 139-149.; Moss 2008, op. cit. note 33.
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Genes and the conceptualisation of language knowledge

ALISON WRAY 1 Abstract While it would be difficult to dispute that individuals vary in their facility with both their native language and with foreign languages, a central tenet of modern linguistics has been that such variation is secondary, and there is a primary level of equality across all individuals. Syntactic theory and sociolinguistic theory have both contributed to the maintenance of this view, and it provides a socially acceptable approach to studying language form and function. However, genes are the authors of both similarity and difference, making their role in language complicated to unpick. The proposed syntactic basis for equality has been a genetically-determined language faculty, which presumably arose early in the modern species and has reliably persisted in all individuals until today. How much fundamental uniformity of language knowledge is there, though? Does it matter if a key feature is not observed in unwritten languages, if there are languages that permit structures that should be prohibited, or if some individuals are less adept at managing purportedly universally understood configurations than others? How might culturally augmented features in language structure be inappropriately influencing claims about what all languages are like? These questions are directly relevant to those engaging with genetics because of the growing opportunities to explore the relative roles of environment and genes in determining aspects of our language knowledge and performance. More generally for society, they present an uncomfortable challenge for how we should handle evidence of genetically-based differences in fundamental language ability, should we find it. 1 Introduction: Individual differences in linguistic ability It is indisputable that there is variation in individuals ability to produce and use language effectively. We have all met the tongue-tied, people who cant remember jokes, pedants, punsters, those who can remember the numbers but not the letters on a car registration plate, loathers of poetry, talented wordsmiths, polyglots, those who struggle to grasp words on the tip of their tongue, diplomatic negotiators, and fluent gossipers. But where does that variation come from? Since so much of our linguistic behaviour is evidently determined by our environmentby our education and experience in particularnaturally we will first look there for explanations of difference between individuals. However, the role of genes is increasingly under examination, particularly now with focus on how genes and environment might interact. 2 This new research offers linguists interesting challenges that extend beyond the domain of language description and modelling, to the heart of how we conceptualise our human linguistic heritage, and how we explain and address diversity.
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1.1 The language faculty One approach to understanding the nature of human language, most strongly championed by Noam Chomsky, ascribes to us all a uniform language faculty (described further in section 3). Universal possession of this faculty means that all human languages are constructed according to its specifications, and this makes them all equally acquirable by children, who use the faculty to navigate a fast and reliable route through their input, to language-specific knowledge. On account of the language faculty, it is, in this approach, desirable to capture the essence of a language system as a logical description of its properties, and this is achieved using the linguists intuitions about what constitutes a grammatical sentence. These intuitions are assumed to represent those of all native speakers (see later discussion of this point in section 7.1). In contrast, language as it is used in communication is considered a poor window on the underlying system, since various effects of production and performance intervene to present a partial and distorted impression of it. 3 Compare how people engage with their personal computers. The language faculty is rather like the operating system, assumed to be the same for a given set of users, and to have a logical shape that can be described. However, people using it, while certainly exploiting aspects of its structure and bound overall to operate within what it permits, may actually use it in rather odd ways that reflect the experience they have had with it, and what they need to achieve. Not only might some aspects of the system not be reflected in their usage at all, but a simple underlying structure may appear very different, even countermanded, in usage, because intervening, less fundamental operations disguise it. Thus, the Chomskian argument is that the linguistic output of speakers is too channelled by circumstantial interventions to be an effective way of understanding the underlying system. The native speakers intuitions, on the other hand, offer relatively direct access to it. Judgments about what sounds right, and how a given sentence can be grammatically re-expressed, reveal complex patterns of, and constraints on, configurations that do not always reflect maximum expediency in the communication of ideas. 4 Theories of language that are based on emergent properties, on the other hand, 5 would either deny, or downplay the importance of, an operating system that is independent of what users do. A more appropriate analogy for them might be how a dance is learned. Someone starts doing some steps, and other dancers, through observation, begin to pick up the patterns. Over time, the novices become the experts, and others pick the dance up from them. There is a system in the sense of a patterned dance, but it does not exist independently of the dancers, and it may change over time. That it always remains a dancethat there are consistent fundamental features such as rhythmic, repeated movements carried out standing upcan be attributed to physical and other characteristics shared by the dancers that are not themselves about dance (eg, being bipedal, having procedural memory), as well as a more general cognitive tendency to latch onto certain kinds of features as central, while others are peripheral. 6 One can see, even from these two very imperfect analogies, that the role of cultural transmission, as opposed to genetic predisposition, is central to debates about
language. The different positions can be characterised by imagining a generation that did not use the computer, or did not observe the dance: what would be left, what could re-emerge, and how similar would it be to what had previously existed? 1.2 Engaging with similarity and variation In this paper I want to explore some of the assumptions and claims about the role of genes in defining the nature of human language. Much has been published on this topic already, and rather than rehearse existing arguments in depth, I shall often simply note their existence and move on. This is because I want to focus on some issues that have been less often brought out, including our social unease when it comes to challenging the entailment of the language faculty account, that all humans have an equal capacity for language at the fundamental level. 7 In section 2, I contextualise the discussion by exploring perceptions of genes as agents of similarity and difference. Sections 3 and 4 deal with claims regarding the uniformity of our fundamental capacity for language, and why it is attractive to maintain this belief, even in the face of potential counter-evidence. In section 5, explanations for the origins of uniformity are considered, and in section 6, I itemise some evidence of variation at the fundamental level. This leads to a testing, in section 7, of the assumptions underpinning the interpretation of apparent evidence for genetically-determined uniformity in language, and the offering of an alternative explanation. Finally, in section 8, I note the current interest in genetic variation in language performance, and consider the extent to which the role of environment in creating the appearance of genetic uniformity may have been under-estimated. 2 Genes as agents of similarity and difference Genes make us the same as each other, and different from each other. At the species level, our genes make us human and other species non-human. At this level, genes explain why a child acquires language while the family dog does not, even though they may be spoken to equally and in not dissimilar ways. The essential humanness of language is not unduly diminished by evidence that apes can make quite a good job of language comprehension 8 and that parrots display, in comprehension and speech, an impressive command of semantics; 9 for there is no real evidence as yet that nonhuman species have grasped the key features of human language structure (see section 3). 10 At the same time, we see our genes as part of the reason why we are different from even our siblings (unless we have an identical twin, in which case differences must be explained another way). Individual characteristics can be the result of a random mutation or copying error in our DNA, but most of them are inherited and have only the appearance of uniqueness, because no one else in the family happens to have expressed the trait. Between the two extremes of shared human-ness and individuality, we also recognise how certain genes, particularly but not only those responsible for visible traits, make us like our family, but different from those outside the family. Extending upwards, we acknowledge that our genes give us visible physical characteristics that make us look more similar to people in some populations in the
world than others. Thus, our perception of the role of the gene contributes to how we construct our personal and social identity as a combination of differences from, and similarities with, others. Where in this picture, then, do we locate differences in peoples language ability? Are they reflections of those genes that make us individualperhaps genes directly determining some aspect of our capacity for languageor are they a superficial, environmentally-determined layer atop fundamental uniformity for language ability? Or both? Generally, there has been a tendency to acknowledge that differences in aspects of our language ability can have a genetic basis, but to view the genetic component as non-linguistic, with linguistic consequences. For instance, poor memory or low concentration could affect the ability fully to benefit from opportunities for learning the finer skills of language presented experientially. Such explanations seem more comfortable for us than proposing that particular genes directly determine why our vocabulary size is different from someone elses, or why we are particularly good, or bad, at learning other languages. Research evidence so far appears to concur. Although a single-point mutation of the FOXP2 gene has been associated with language deficits, the genes role seems to be in regulating brain development, with knock-on effects for language, rather than directly supporting articulation or grammar. 11 It may be feasible to explain everything about language in terms of the interaction of environmental influences and genetically-endowed abilities that are not of themselves specifically linguistic. What is uniform about how we engage with linguistic structure would, then, be a natural consequence of how these factors interact. However, proponents of the language faculty believe otherwisethe faculty is construed as a uniform, language-specific genetic inheritance. 3 Structural arguments for language uniformity Over some 50 years, Noam Chomsky has maintained that humans possess a language organ whose basic character is an expression of the genes. 12 According to Chomsky, our basic genetic endowment determines an initial state of the language faculty, a language acquisition device that takes experience as input and gives the language as an output that is internally represented in the mind/brain. 13 The language faculty is logically necessary, Chomsky claims, to explain how children acquire their first language with such extraordinary speed and consistency, irrespective of the quantity and quality of the input and, in particular, how they are able to infer certain grammatical patterns on the basis of only negative evidence. The faculty ensures that children know what to look for in the input, in order to make structural sense of it. 14 In recent accounts just two properties lie at the heart of this universal knowledge of language grammar: structure dependence and recursivity. After briefly reviewing the nature of each, we shall also consider one of the properties claimed to be consequential on them, Subjacency.
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3.1 Structure dependence In structure dependence, small units of language combine into larger units, and units maintain their underlying integrity if the sentence is reformulated. To briefly exemplify, turning the statement in (1) into the question in (2) entails the recognition that the was that moves to the start of the question is the second one in (1), not the first one. The clause that was seen in the River Thames is a unit embedded in another unit, The whale was a juvenile. The question formation involves this outer clause, not the embedded one, so that it is the verb in the outer clause that is fronted, not its identical counterpart in the embedded clause. 1) The whale that was seen in the River Thames was a juvenile. 2) Was the whale that was seen in the River Thames a juvenile? Chomsky argues that if children did not come to language acquisition already knowing the principle of structure dependence, they could all too easily infer, from simpler examples such as (3) that the rule was move the first verb to the front, an adequate way to generate (4), but also leading to the creation of the ungrammatical (5). 15 (The asterisk on (5) indicates that the sentence is classified as ungrammatical). 3) The whale was a juvenile. 4) Was the whale a juvenile? 5) *Was the whale that seen in the River Thames was a juvenile? The ubiquity of structure dependence in language, and its possible non-linguistic precursors in our species, as indicated by counterparts in animal cognition, 16 mean it is hardly contentious to suppose that humans possess some sort of innate disposition towards it. However, many, including Newmeyer, still see it as specific, in its instantiation, to the language faculty: The structure dependence of grammatical rules might well have its evolutionary antecedence in some general human (or, more likely, biological) preference for structural solutions to complex problems. But structure dependence in grammar is a highly specific adaptation of this general preference. 17 3.2 Recursivity Recursivity is the single feature identified by Hauser, Chomsky and Fitch as making human language unique. 18 Recursivity in language means that the output of one grammatical operation can act as the input for another. The effect is that there is no logical bar on the complexity of sentences. It is, for instance, grammatical to embed one clause inside another, then another inside that, another inside that, and so on (610). 19 6) The mechanic tells fortunes. 7) I know the mechanic tells fortunes. 8) I know the mechanic the tailor saw yesterday tells fortunes. 9) I know the mechanic the tailor who makes those suits saw yesterday tells fortunes. 10) I know the mechanic the tailor who makes those suits you were thinking of buying saw yesterday tells fortunes.
3.3 Subjacency: a consequential property In Chomskys models until the mid-1990s, certain additional properties of language were considered universals in their own right. One of them was Subjacency. Subjacency constrains grammatical relations arising from embedding. When one clause is embedded inside another, grammatical dependencies can arise across them. An item in one clause may cross-refer to an item in another; an item in one clause may be deleted because it also exists in another, setting up a dependency between the explicit item and the gap where the deleted item was; or an item may be moved into another clause in order to fulfil a particular function, as in English when wh-questions are created. Subjacency prevents the linked itemsin the case of a wh-question, the moved wh-word and its original location (or trace)becoming impossible to track, by constraining the amount and type of structural material that may intervene. The effect is to allow (12) but not (13) as grammatical developments of (11), even though (13) is simply a wh-fronted version of (14). 11) Elsie bought a coat. 12) What do you believe (that) Elsie bought? 13) *What do you believe the claim that Elsie bought? 14) You believe the claim that Elsie bought what? Chomskys Minimalist Program simplified the notion of Universal Grammar, by making principles like Subjacency a logical consequence of the two core features structure dependence and recursivityplus language-specific rules. 20 Thus, the learning child minimally needs a notion of hierarchical structure plus an understanding of transformations and constraints on them. 21 Adherence to Subjacency is ensured if the child knows that the progressive stages by which a transformed sentence such as a wh-question is constructed must occur sequentially, in successive cyclic movements, each of which cross a minimal unit of structure. 22 Violations of Subjacency occur when one or more of the individual cycles cannot be completed, on account of an item occupying a slot that must be empty when that cycle takes place. In section 6 we shall consider the claim that Subjacency cannot be construed as universal since it does not manifest in all languages. 4 Social arguments for uniformity Although syntactic models of language knowledge and sociolinguistic descriptions of language behaviour have generally had little to say to each other, they have common socio-political foundations. Sociolinguistic theory has maintained over many years that varieties spoken by uneducated groups, typically viewed by the establishment as aberrant consequences of ignorance, are in fact no less complex or expressively rich than the standard variety. 23 These observations are consistent with the egalitarian Chomskian position: we all start with the same genetically endowed language faculty and use it to treat our input. Since our language faculty obliges us to shape our input data in particular ways, it follows that all output will be of the same fundamental complexity. Therefore, while socially imbued contrasts between languages and varieties cannot be denied, they are only that. Change the social conditions, and the
variety viewed as most ignorant could become the one considered most correct and desirable. It is clearly socially problematic to suggest that one speaker group is in any way fundamentally disadvantaged for language relative to another. 24 Socially induced differences (education provision, access to books, cultural priorities) can be put right through social policies. It would be different indeed to suggest, for instance, that members of a particular group had encoded in their genes a different type of language faculty, that predisposed them to lesser, or greater, capability for language. As with intelligence, 25 language ability is an invisible and contingent trait: it is not known unless it is measured, and it is defined according to particular social values. Such traits are particularly socially sensitive because of the ease with which their presence can be inappropriately inferred by association with a proxy, visible trait such as skin colour, age, gender or disability. The association of invisible traits with visible ones is invidious because unless both are equally ubiquitous (and anything socially interpreted will tend not to be) the one is not a reliable index of the other. To put it crudely, it is socially unacceptableand for good reasonto look at someones appearance and infer thereby that they will be less intelligent or a less able language user than someone else. The uniformitarian perspective on language arose in response to racialist attitudes, whereby it was presumed that the noble savage possessed a lesser (or occasionally greater) capacity for language than the European, and that different races could be located at different points on a directional evolutionary continuum. 26 It is anathema to modern western society that anything construed as desirable should be entirely unattainable, and thus much more comfortable to downplay any notion of fixed ceilings of achievement, whether associated with random individuals, family groups, classes or, most undesirably of all, races. 27 Yet genetics research is increasingly likely to demand answers to difficult questions. In the account above I have focussed on the least desirable scenario, whereby some genetically-determined variation creates inequality. That is, where some populations are viewed as better at language, in some sense, than others, in a way that parallels the claims for systematic differences in IQ levels. However, not all differences entail inequality, and one line of recent research indicates the scope for challenging the notion of uniformity without an associated social stigma. Research by Dediu and Ladd 28 suggests that a particular pattern of genetic variation (derived haplogroups of two genes) explains the distribution of tone languages around the world. Tone languages use patterns of pitch change to differentiate meanings. Dediu and Ladd propose that [t]hose areas of the world where the new alleles are relatively rare also tend to be the areas where tone languages are common, 29 and that the relationship is causalthe genetic structure of a population can exert an influence on the language(s) spoken by that population. 30 They hypothesise that the genetic effects on brain structure determine how tone is handled during the process of language acquisition, with an impact, in heavily affected populations, on the culturally transmitted linguistic code. That is, languages spoken by populations in which many individuals have some difficulty in processing tone will tend to lose their tonal
features. They are careful to note that there is no evidence that tone itself confers any advantage or disadvantage on speakers, 31 so this particular effect should be socially neutral. However, we must not forget that society often interprets variation judgmentally, and where systematic difference is once found, prejudice may follow. 5 Explanations of uniformity Chomskys claim that all humans possess the same fundamental language knowledge draws us inexorably to the question of when and how that knowledge arose, and how it is that humans today still all have it. The most plausible answer to the first part of the question is that it arose in the small sub-population of humans whose descendents we all are, and that possessing it gave the ancestral sub-population a distinct survival advantage over contemporaries without it. In order to avoid the complications of polygenesis, 32 we assume the language faculty arose once only, some time before modern man dispersed out of Africa around 100,000 years ago. 33 As to explaining its uniformly reliable persistence, there are at least three options. One is that selection pressures ensure the failure of anyone without the language faculty to survive and reproduce. Another is that the language faculty, while less than crucial for survival on its own, is tied into other basic human functions without which an individual could not survive and reproduce. A third is that the genetic basis of the language faculty is highly conserved, that is, remarkably resilient to mutation. 34 It is for others to weigh the plausibility of these and other options. It need only be noted here that such evolutionary accounts are predicated on the assumption of uniformity today, so evidence challenging the extent of that uniformity (see section 6) potentially impacts on our understanding of what evolved and how. 35 6 Evidence for variation What sort of variation in language knowledge or performance would directly challenge the claim that we have a genetically-endowed language faculty? Although, as we shall see in section 8, there is place for examining the relative roles of genes and environment in the variation found across a wide range of aspects of language knowledge and performance, that agenda arises separately, and somewhat independently, of the claim for a language faculty. For the present, therefore, the question is whether variation can be adduced in relation to the language knowledge that the innateness accounts have construed as immutable. As we saw in section 3, this knowledge relates to two core features of language, structure dependence and recursivity, and a range of consequential features, including Subjacency, previously identified as central to Universal Grammar. Before Subjacency and other similar principles were down-graded it was reasonable to argue that if one could find a language without Subjacency, one had found evidence that the theory of Universal Grammar was invalid. However, Newmeyer 36 promotes the weaker version of UG theory that the Minimalist Program makes possible. It is unproblematic to find languages without Subjacency, so long as this is only because there is no scope for it to apply (eg, because the language does not use sufficiently
complex embedding). However, it is vital for the theory that when the language develops the additional clausal complexity that provides the forum for Subjacency to apply, then it will apply. The weak Universal Grammar hypothesis challenges its opponents to offer a more compelling kind of evidence than simply the absence of Subjacency in languages without multiple embedding, eg: i) Evidence of the grammatical acceptability of Subjacency violations in languages that do have adequate levels of embedding; ii) Evidence of languages failing to apply recursion, even when expressing appropriate semantic dependencies; iii) Evidence that individuals given examples of complex sentences cannot reliably understand them; iv) Evidence of languages failing reliably to demonstrate structure dependence. There is not, to my knowledge, any instantiation of (iv), though it must be borne in mind that the assumption of structure dependence is so basic a notion to us, that it would be difficult to describe a new language without doggedly pursuing the expectation of it, even if it was not there. 37 Meanwhile, Wray 38 provides (incidentally) a means of explaining away any examples that appear at odds with structure dependence, by proposing that communication is not always reliant on rulebound forms. Formulaic expressions can become and remain irregular by being processed as single lexical entries. The other three proposed types of evidence are apparently attested. Regarding (i), Culicover notes that there are languages such as Italian, Swedish and Icelandic in which systematic violations of Subjacency are possible, in the sense that sentences which would be judged ungrammatical in English are judged grammatical in these languages. There is evidence that it does not even hold uniformly for English. 39 In relation to (ii), Everett 40 has claimed that Pirah, a language spoken in the Brazilian Amazon, does not display recursionit has no embedding. Less extreme claims have been made regarding other languages. Mithun suggests that [l]anguages and speakers vary considerably in the exploitation of this syntactic device 41 and, like Ong, 42 she sees subordination as a feature of writing rather than speech. 43 Kalmr 44 reports a marked increase in grammatical subordination in Inuktitut after decontextualised writing, and translation from English, became more common. In the weaker version of the Universal Grammar hypothesis, the absence of embedding is inconsequential if, on account of having no written tradition, for instance, the relevant semantic dependencies are not expressed at all. But Everett proposes that Pirah does express the meanings that other languages achieve through embedding, and this constitutes one part of his claim that Pirah stands outside the scope of predicted possible languages. Evidence of variation in peoples capacity to understand complex embedded sentences (iii) has been offered by Chipere. 45 His experimental stimuli were sentences like (15),
for which he solicited both direct repetitions and answers to comprehension questions (eg, What does the doctor know? and What surprises Tom?). 15) The doctor knows that the fact that taking good care of himself is essential surprises Tom. He found non-graduate native speakers less able than native and non-native speaker graduates to take into account the various parts of the structure when responding to comprehension questions. Since the non-native speaker graduates actually gave the most accurate responses to some questions, Chipere suggests that explicit instruction in the grammar of English (of which the non-native graduates would have experienced most and the non-graduate native speakers least) is of assistance in understanding complex sentences. He also found that individuals unable to remember or understand the stimuli responded well to training, explaining his results by means of Ericsson & Kintschs proposal that in skilled activities, acquired memory skills allow [the] products [of interim operations] to be stored in long-term memory and kept directly accessible by means of retrieval cues in short-term memory. 46 Chipere suggests that training in how to understand complex sentences supports the development of a rule-based strategy for unpacking them, without which it is more natural to interpret them by analogy, using syntactic formulae, impose[d] top-down on the input. 47 Possible implications of Chiperes proposal are considered in section 8. 7 Causes and effects of variation 7.1 Cultural enhancements of language If one believes that all languages are essentially equal in complexity, all the natural product of a species-wide language capacity, it is not unreasonable to examine only a small number of languages in order to identify the features of that capacity. However, for as long as these beliefs are only beliefs, it is obviously necessary to ensure that there is no bias in the sample, lest one attribute universality to some feature that is a secondary accretion peculiar to the sampled languages. Grace 48 outlines dangers inherent in a culture-centric approach to language description. English, the language most often drawn upon for modern linguistic analysis, is in many respects an artificial language. It has a long history of literary development and of standardisation. While it remains natural in the sense that native speakers acquire it, the version they acquire is frequently treated as culturally inadequate, so that additional training, through education, is required to master the niceties of specific varieties elevated as correct. Since the features of this correctness have accreted over timemostly as expressions of preferences imposed by intellectual adults 49 and often emulating patterns in Latin and Greekthere is no reason why the standard forms of English, locked into writing, though then extrapolated back as an educated spoken code, should reflect all and only natural patterns. The kinds of sentences at the heart of Chomskian accounts of complex grammar might therefore be unnatural.
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In an application of Graces ideas to the question of language evolution, Wray & Grace 50 offer a model of how cultural demands, particularly the need to talk to outsiders, augment a less ambitious default version of language structure in the direction of greater explicitness and regularity. One outcome might be a greater use of embedding for encoding complex meaning relationships in a retrievable way. Wray & Grace propose that for most of human evolution, languages have not been under the cultural pressure that augments their form in these directions. 7.2 Genetic variation over time The evolutionary origin of language also offers another potential explanation for variation between languages at the fundamental level. Let us suppose that a dedicated language faculty did arise in our species some time around or after 200,000 years ago. Our earliest modern ancestors, let us imagine, understood the principles of structure dependence and recursion. Let us further suppose that they understood structural relations in multiply embedded sentences after the movement of constituentseven though their spoken language(s) never provided a context in which to exercise that knowledge. Although this provides a uniform starting point for our species, under what circumstances would that uniformity remain? Two hundred thousand years is a very long time for a trait to be maintained with 100% reliability across the human population, when it is not in use, and when no disadvantage ensues from its absence. 51 Why, over the many millennia during whichif Wray & Grace are rightembedding was barely in use, might not some humans emerge, who by virtue of slightly different innate language knowledge, or on account of some difference in how they approach information processing and storage, find embedded structures more difficult to compute? At the time, no one would notice, whether it were a trait in random individuals across all populations, or one passed down in family lines. In theory, it could even come to characterise one gender more than the other, or a particular coherent populationwe are back on socially sensitive ground. My aim is not particularly to suggest that the universality of an original language faculty actually has been undermined by silent genetic variation, so much as to indicate that we need to explain why it could not have been. In actual fact, were we to become satisfied that a feature of language such as recursion was not equally represented in the innate knowledge of all individuals, we should probably not wish to hypothesise the undoing of something originally ubiquitous at all, unless there was no other way to explain the origins of its vestiges in the species. Even so, the idea that we have innate linguistic knowledge the detail of which has diverged in the course of evolution is too important to set aside, and it raises interesting issues for consideration, as explored in the final section. 8.0 Less than black and white A few years ago people talked simplistically of a language gene, and that made it easy to conceptualise all humans as equally linguistically endowed. But the accepted view now is that our capacity for language is determined by many genes, many or all
of which might exist in variant forms. Whether defining language as a complex trait obviates the possibility that there lies at their heart some special, invariant faculty dedicated to language is a topic of continuing debate. As for perceptions of the role of the environment, they too have become more complex. Although it remains likely that much of the variation in language and languages is culturally-determined and maintained, it is now increasingly recognised that genes and environment interact. For example, in epigenetics the expression of the gene is determined by an environmental trigger. 52 Nettle 53 tentatively suggests another kind of gene-environment interaction in relation to Dediu and Ladds findings for tone languages, described earlier. Where they propose that a particular genetic expression may have influenced the properties of a pattern in the languages spoken by the affected people, Nettle additionally proposes that, in return, the language features could have led to positive selection for that gene expression in subsequent generations. 54 The more complex the genetic and environmental factors determining language are seen to be, the harder it is to be sure on what basis we can safely judge a feature of language to be truly invariant across all normal humans. Most research discusses whether or not the phenomenon of language can be explained without recourse to a universal language faculty, but in this paper I have focussed on two different questionswhether the faculty, if it did exist, could have variant forms, and whether, if it did, we would be able to tell. Specifically, I have explored the possibility that our cultural engagement with language influences our linguistic knowledge at the most fundamental level, and I have considered whether our evolutionary development could have supported a bifurcation (or more) in peoples innate knowledge about language, as the result of genetic variation. Were both true, it could mean that what one person did through innate knowledge, another could learn to do. Chiperes 55 work offers one candidate type of knowledgethe processing of complex embedded structures using long term memory. 56 Inherited predispositions to handle complex embedded structures without, versus only with, training would constitute a very subtle distinction of no consequence, until cultural practices arose that prized the ability to encode and decode complex language, while the associated educational system was less than vigilant about teaching that ability to those not immediately adept. Such circumstances could play a role in creating and sustaining differences in social and material attainment. Since the skill was learnable, bootstrapping would be entirely feasible, but effort would be entailed if one were to match the natural abilities of those with the innate disposition. Irrespective of the plausibility of this particular scenario, variation between individuals in relation to what we term language aptitude or flair for language does exist and may not be easily explained in terms of environment alone. For this reason there is an urgent need for research into the genetic basis for the many aspects of variation in language knowledge and aptitudeas now being undertaken for Specific Language Impairment, 57 and through twin studies. 58,59 Twin studies can help separate
out the genetic contribution to variation from that partly or entirely due to environment. Evidence suggests, however, that not only postnatal but also perinatal environmental factors play a role in how language develops, 60 a fact that complicates assumptions about genetically identical input being expressed identically in different individuals even in the early years of life. Establishing the role of genes in determining our language abilities is only one part of the challenge, however. The other is learning to cope with all of the possible outcomes of such research. A mature society needs a means of dealing with the discovery of genetically-based differences in capabilities that, on strongly defensible cultural grounds, we would rather believe were fundamentally invariant. Acknowledgements The Cardiff symposium What is special about the gene? provided the impetus for developing many of the ideas in this paper. I am grateful to Stephen Pattison and Andrew Edgar for their invitation to participate. The paper has benefited from helpful comments and advice from Alison Sealey, Naomi Wray, and two anonymous referees, and from discussions with Tess Fitzpatrick, George Grace, Eugne Mollet and Mike Wallace, to all of whom I express my thanks.
Centre for Language and Communication Research, School of English, Communication and Philosophy, Cardiff University, UK wraya@cf.ac.uk 2 For some discussion, see D. Nettle. Language and genes: a new perspective on the origins of cultural diversity. Proceedings of the National Academy of Sciences 2007; 104 (26): 10755-10756. 3 Linguistic theory is concerned primarily with an ideal speaker-listener, in a completely homogeneous speech-community, who knows the language perfectly and is unaffected by such grammatically irrelevant conditions as memory limitations, distractions, shifts of attention or interest, and errors (random or characteristic) in applying his knowledge of the language in actual performance. N. Chomsky. 1965. Aspects of the Theory of Syntax. Cambridge, MA: MIT Press, p.3. 4 Examples of constraints that do not seem to translate into use include the one that outlaws *The asleep girl as a re-expression of The girl is asleep (compare The expensive car as a re-expression of The car is expensive). Constructions that are attested in usage but are outlawed by intuition include the one underlying What's the one episode that you wrote, that when you saw it, it just blew you away? (interview with Ronald D. Moore, writer of Roswell, www.scifi.com/sfw/issue234/interview.htlm, accessed 27.01.08). A striking example of a structure that Generative grammars predict but which is very rarely attested is gapping, eg, I ate fish, Bill rice and Harry roast beef, which Tao & Meyer (2006) describe as one of the most extensively studied syntactic constructions in English (p.129) but one that is very rarely found in corpus data. In the ICE-GB corpus (1 million words) they found 17,629 clauses that were structured appropriately to permit gapping, but only 120 (0.7%) that actually had it. 5 eg, Construction Grammar. See for instance, A.E. Goldberg. 2006. Constructions at Work, Oxford: Oxford University Press, chapter 1. 6 Chomskian models do not exclude a role for general cognitive influences, but do view them as complementing the dedicated language faculty. 7 The assumption of uniformity in humans leads to assumptions about uniformity in languages. It is claims like we find the same basic structural properties in every human language, S.R. Anderson. 2004. Doctor Dolittles Delusion. New Haven, CT: Yale University Press, p.199 that are increasingly being challenged (see later). The tendency for an idea to become commonly accepted without adequate evidence is exemplified by Pullum and Scholz in relation to another common claim in linguistics, that _____________ Genomics, Society and Policy, Vol.4, No.1 (2008) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com 70
languages have infinite expressional capacity. G. Pullum and B. Scholz. 2008. Language and the infinitude claim. http://ling.ed.ac.uk/~gpullum/bcscholz/Infinitude.pdf, accessed 28.01.08. 8 eg, K.E. Brakke and E.S. Savage-Rumbaugh. The development of language skills in bonobo and chimpanzee I: comprehension. Language and Communication 1995; 15 (2): 121-148. 9 eg, I.M. Pepperberg.1999. The Alex Studies. Cambridge, MA. Harvard University Press. 10 Anderson, op. cit. note 7. 11 eg, F. Vargha-Khadem et al. FOXP2 and the neuroanatomy of speech and language. Nature Reviews Neuroscience 2005; 6: 131-137. Language deficits in the KE family seem to include articulatory problems and difficulty applying the agreement rules on verbs and nouns. They have been linked to a single base substitution in FOXP2, on Chromosome 7. 12 N. Chomsky. 2000. New horizons in the study of language and mind. Cambridge: Cambridge University Press, p.4 13 Chomsky, op. cit. note 12. 14 As part of his energetic argument against the notion of a genetically-determined language faculty, Geoffrey Sampson (The Language Instinct Debate, London: Continuum, 2005) counters each of Chomskys key claims in turn, arguing that they are predicated on invalid assumptions about the nature of the input presented to children and the bases on which it could result in the kind of output they produce. Taking a different approach to the challenge, G. Pullum & B. Scholz, Empirical assessment of stimulus poverty arguments. Linguistic Review 2002; 19 (1-2): 9-50, identify the evidential requirements for arguing for or against innate knowledge. 15 N. Chomsky. 1976. Reflections on Language, London: Fontana/Collins, p.33ff. 16 J.R. Hurford, 2007. The origins of meaning. Oxford, Oxford University Press. 17 F. Newmeyer. 2005. Possible and probable languages. Oxford: Oxford University Press, p. 11-12. 18 M. Hauser, N. Chomsky and W.T. Fitch. The faculty of language: what is it, who has it, and how did it evolve? Science 2002; 298, 22/11/02, 1569-1579. 19 However, see Pullum and Scholz 2008, op. cit. note 7 for reasons why this capacity for infinite embedding has been generally overstated. 20 Newmeyer, op. cit. note 17, chapter 3. 21 W. Hinzen. 2006. Mind Design and Minimal Syntax. Oxford: Oxford University Press, p.196. 22 Hinzen, op. cit. note 21, p.198. 23 eg, W. Labov. The logic of non-standard English. In J. Alatis ed. Georgetown Monographs on Languages and Linguistics 1969; 22, 1-44. 24 The focus here is on the normal population (though normality is, of course, a social construct). See a later note for comments on abnormal language. 25 See, for instance, the recent furore over claims by James Watson of differences in intelligence between black, white and Asian people: Times Online. 2007. Black people less intelligent, scientist claims. http://www.timesonline.co.uk/tol/news/uk/article2677098.ece 26 G. Radick. 2008, The Simian tongue: the Long Debate about Animal Language. Chicago: University of Chicago Press, chapter 5. 27 The concept of race is generally recognised to be a social construct that does not map effectively onto the biological evidence. See, for example, L. Lieberman and F.L.C. Jackson. Race and three models of human origin. American Anthropologist 1995; 97 (2): 231-242. 28 D. Dediu and D. R. Ladd. Linguistic tone is related to the population frequency of the adaptive haplogroups of two brain size genes, APSM and Microcephalin. Proceedings of the National Academy of Sciences 2007; 104 (26), 10944-10949. 29 Dediu and Ladd, op. cit. note 28, p.10945. 30 Dediu and Ladd, op. cit. note 28, p. 10946. 31 Dediu and Ladd, op. cit. note 28, p. 10946. 32 I use the term polygenesis as linguists do, to refer to the independent emergence of language more than once in the human species. It contrasts with monogenesis, a single emergence event, often assumed to entail both the cognitive capability for language processing and the first linguistic code, from which all subsequent languages have developed (though there is certainly scope to account for these events separately). Polygenesis has a different meaning in genetics, which is not intended here. 33 Estimates tend to assume the emergence of modern man, with language, 200,000 to 150,000 years ago, in Africa. There are other hypotheses too, however, including a much later date coinciding with _____________ Genomics, Society and Policy, Vol.4, No.1 (2008) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com 71
the first cultural evidence of language (eg, religious rituals, cave art). But language emergence after the dispersal from Africa obviates a monogenetic origin for language, and polygenesis naturally weakens the claim for uniformity across all languages. 34 Vargha-Khadem et al. op. cit. note 11, p. 137. 35 Of course, not all linguists by any means believe that there is a language faculty as such at all, and all linguists accept that the language package as a whole (including speech, naming, remembering, assigning thematic roles to participants in clauses, etc.) has entailed the presumably independently motivated evolution of many different abilities. 36 eg, op. cit. note 17. Also F. Newmeyer. 2002. Uniformitarian assumptions and language evolution research. In A. Wray (ed.) The Transition to Language. Oxford: Oxford University Press, 359-375. 37 Compare Boas advice to the anthropologist, to divest himself entirely of opinions and emotions based on the peculiar social environment into which he is born. F. Boas. The Mind of Primitive Man. Journal of American Folk-Lore 1901; 14 (52), 1-11. 38 A. Wray. 2002. Formulaic Language and the Lexicon. Cambridge: Cambridge University Press. 39 P. Culicover. 1996. Adaptive Learning and Concrete Minimalism. In C. Koster and F. Wijnen, eds, Proceedings of the Groningen Assembly on Language Acquisition. Groningen Assembly on Language Acquisition (GALA 1995), Center for Language and Cognition, Groningen, 165-174. Available at http://www.ling.ohio-state.edu/~culicove/Publications/GALA.pdf, last accessed 28.01.08 40 D. Everett. Cultural constraints on grammar and cognition in Pirah. Current Anthropology 2005; 46, 4: 621-646. 41 M. Mithun. How to avoid subordination. In Proceedings of the Tenth Annual Meeting of the Berkeley Linguistics Society 1984; 493523, p. 509 42 W.J. Ong. 1982. Orality and Literacy: The Technologizing of the Word. Methuen, London. 43 Some culturally developed types of spoken language, such as oral epics, may also display structural complexity. Oral literature is characterised by repetition, a creative mix of familiar formulae and new material, and opportunities for both speaker rehearsal and multiple hearings; see discussion in A. Wray. forthcoming. Formulaic Language: Pushing the Boundaries. Oxford: Oxford University Press. 44 I. Kalmr. 1985. Are there really no primitive languages? In D.R. Olson, N. Torrance and A. Hildyard eds. Literacy, Language and Learning. Cambridge: Cambridge University Press, 148166. 45 N. Chipere. 2003. Understanding complex sentences. Basingstoke: Palgrave. 46 K.A. Ericsson and W. Kintsch. 1995. Long term memory. Psychological Review 102, 2, 211245, p.211. 47 Chipere, op. cit. note 45, p.180. 48 G.W. Grace Collateral damage from linguistics? 3: The role of culture-centrism. Ethnolinguistic Notes 2002; 4 (23) http://www2.hawaii.edu/~grace/elniv23.html, accessed 28.01.08. 49 The difference between how adults approach the identification of language patterns, compared with children, is explored at length in Wray op. cit. note 38. 50 A. Wray and G.W. Grace. The consequences of talking to strangers: Evolutionary corollaries of socio-cultural influences on linguistic form. Lingua 2007; 117, 543578. 51 It is, of course, possible that the trait, though not used for language, was vital for something else, such as organising thought, or planning actions. This argument, however, entails that the trait is not part of a dedicated language faculty. 52 eg, M.F. Fraga et al. Epigenetic differences arise during the lifetime of monozygotic twins. Proceedings of the National Academy of Sciences 2005; 102 (30): 1060410609. 53 Fraga, op. cit. note 52. 54 This process is known as the Baldwin effect. 55 Chipere, op. cit. note 45. 56 Dediu and Ladd, op. cit. note 28, offer another. As with the present account, they propose that the variation would not be sufficient to disadvantage an individual. Their account explores the effect on languages of many individuals in a population exhibiting a particular trait, something that could logically extend to the present scenario too. 57 Abnormalities in language can take many forms, and they are generally attributed to impairments in one or more component of the complex package that supports the hypothesised language faculty (eg, auditory processing, memory, planning, production processing, social interaction, reading). For an overview, see G. Barnby and A. Monaco. 2007. Speech and language disorders. In A. Wright and N. _____________ Genomics, Society and Policy, Vol.4, No.1 (2008) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com 72
Hastie, eds. Genes and Common Diseases: Genetics in Modern Medicine. Cambridge: Cambridge University Press, pp. 469-487. So far there has been no convincing evidence of impairment to just a language faculty in the narrow sense defined in this paper, though it is far from clear what one should look for in identifying an affected person. 58 For a comprehensive review of published studies, see K. Stromswold. The heritability of language: a review and meta-analysis of twin, adoption, and linkage studies. Language 2001; 77, 4, 647-723. 59 My own current project (April 2007- Sept 2008), funded by the UK Arts and Humanities Research Council and in collaboration with the Twin Study at the Queensland Institute of Medical Research, is applying a wide range of language profiling techniques to essays written by identical and non-identical twins in a state-wide school examination. 60 K. Stromswold. Why arent identical twins linguistically identical? Genetic, prenatal and postnatal factors. Cognition 2006; 101, 333-384.
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Author Biographies
David Amigoni is Professor of Victorian Literature at Keele University, where he is also Director of the Research Institute for the Humanities. He researches the literature and science relation in the Victorian period and his monograph Colonies, Cults and Evolution: Literature, Science and Culture in Nineteenth-Century Writing was published by Cambridge University Press in 2007. d.amigoni@keele.ac.uk Roberta Bivins is Associate Professor in the History of Medicine at the University of Warwick, UK. She is currently researching the impact of postcolonial immigration on medical research and healthcare delivery in the US and the UK. Other work has examined the cross-cultural transmission of medical expertise. bivinsre@Cardiff.ac.uk Andrew Edgar is Senior Lecturer in Philosophy in the School of English Communications and Philosophy at Cardiff University. His research has been in twentieth century German philosophy and in the philosophy of medicine. He is editor of the journal Health Care Analysis. edgar@Cardiff.ac.uk Tim Ingold is Professor of Social Anthropology at the University of Aberdeen. He has carried out ethnographic fieldwork among Saami and Finnish people in Lapland, and has written extensively on comparative questions of environment, technology and social organisation in the circumpolar North. Other interests include evolutionary theory in anthropology, biology and history; the role of animals in human society; human ecology, language and tool use; and environmental perception and skilled practice. He is currently writing and teaching on the comparative anthropology of the line, and on the interface between anthropology, archaeology, art and architecture. His latest book, Lines: A Brief History (Routledge), was published in 2007. tim.ingold@abdn.ac.uk Lenny Moss is Associate Professor of Philosophy at the University of Exeter. Trained in both cell biology and philosophy, his current research interests include: a renewal of the enterprise of philosophical anthropology based upon a new synthesis and dialectical interpenetration of philosophy and the empirical sciences; a philosophical reconstruction of the history of philosophy from the perspective of an expressivist anthropology; the philosophical elucidation of a phenotype-first biology and its implications for a general philosophy of nature guided by the idea of natural detachment as an immanent teleology. His 2003 book What Genes Cant Do (MIT) has just been published in Japanese. Lenny.Moss@exeter.ac.uk Stephen Pattison is Professor of Religion, Ethics, and Practice in the Department of Theology and Religion at the University of Birmingham. He is joint co-ordinator with Andrew Edgar of the interdisciplinary humanities project, 'The Meanings of Genetics'. s.pattison.1@bham.ac.uk Alison Wray is a Research Professor in Language and Communication at Cardiff University. Her particular interests are the psychological and social determiners of formulaic language use and the evolution of language, on both of which topics she has
_____________ Genomics, Society and Policy, Vol.4 No.1 (2007) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com 74
published widely. Her present empirical projects focus on new approaches to profiling variation in language performance, as an index of linguistic knowledge and of learning and processing strategies. wraya@Cardiff.ac.uk
_____________ Genomics, Society and Policy, Vol.4 No.1 (2007) ISSN: 1746-5354 ESRC Genomics Network. www.gspjournal.com
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Editorial: What Is Special About The Gene?

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VOLUME 4, NUMBER 1 (APRIL 2008) SPECIAL ISSUE: WHAT IS SPECIAL ABOUT THE GENE?

GUEST EDITORS: ANDREW EDGAR & STEPHEN PATTISON

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Editorial: What is special about the gene?

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What is special about the gene? A literary perspective

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Hybrid Vigour? Genes, Genomics, and History

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When biology goes underground: genes and the spectre of race 1

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The Meanings of the Gene and the Future of the Phenotype

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