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Herbicide Resistance: A Threat to Herbicide Utility and Sustainability

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 Advances
In
Agriculture Sciences
Volume - 3

Chief Editor
Dr. R.K. Naresh
Professor, Department of Agronomy, College of Agriculture, Sardar
Vallabhbhai Patel Univ. of Agri & Tech, Meerut-250110, Uttar Pradesh,
India

AkiNik Publications
New Delhi
Published By: AkiNik Publications

AkiNik Publications
169, C-11, Sector - 3,
Rohini, Delhi-110085, India
Toll Free (India) – 18001234070

Chief Editor: Dr. R.K. Naresh

The author/publisher has attempted to trace and acknowledge the materials

reproduced in this publication and apologize if permission and
acknowledgements to publish in this form have not been given. If any material
has not been acknowledged please write and let us know so that we may rectify
it.

© AkiNik Publications
Pages: 129
ISBN: 978-93-88112-21-5
Price: ` 515/-
Book DOI No.:
 Contents

Chapters Page No.

1. Present Status and Future Prospectus of Production and

Detection of GM Crop Seeds 01-21
(Narayana Swamy K.C, Harish M.S)

2. RNA Interference and Its Applications in Crop Improvement 23-32

(Loyavar Ramchander, P. Sudheer Kumar, V. Umesh Kumar, Nellipalli Vinod
Kumar)

3. Soil Fertility Management in Organic Farming System 33-43

(Paila Harikrishna)

4. Role of Semiochemicals in Insect Pest Management for

Sustainable Agriculture 45-53
(K Deekshita, Mounica D)

5. Concept of Soils 55-64

(M.K. Jat, Abha Tikkoo, R.S. Dadarwal)

6. Soil Health and Climate Change 65-74

(Jayswal P.S, Sondarva K.N)

7. Phytoremediation of Heavy Metals: A Green Technology to

Clean Environment 75-87
(Tikendra Kumar Yadav, J.K. Singh, Nupur Sharma, Satya Prakash
Vishwakarma)

8. Biology and Population Dynamics of Solenopsis Mealybug

Parasitoid, Aenasius Bambawalei Hayat (A. Arizonesis
89-112
Girault)
Vijaya, Dharmendar Singh

9. Herbicide Resistance: A Threat to Herbicide Utility and

Sustainability 113-129
Sudershan Mishra, Dr. S.K. Guru, Nitin Kumar, Prinsa Ramola, Babita Joshi
 Chapter - 9
Herbicide Resistance: A Threat to Herbicide Utility and
Sustainability

Authors
Sudershan Mishra
MSc. Agriculture in Plant Physiology, ICAR JRF,
Dept. of Plant Physiology, College of Basic Sciences and Humanities
GB Pant University of Agriculture and Technology
Pantnagar, Uttarakhand, India
Dr. S.K. Guru
Professor, Dept. of Plant Physiology,
College of Basic Sciences and Humanities
GB Pant University of Agriculture and Technology
Pantnagar, Uttarakhand, India
Nitin Kumar
Ph.D Plant Physiology, Dept. of Plant Physiology,
College of Basic Sciences and Humanities
GB Pant University of Agriculture and Technology
Pantnagar, Uttarakhand, India
Prinsa Ramola
Ph.D Student, Dept. of Plant Physiology,
College of Basic Sciences and Humanities,
GB Pant University of Agriculture and Technology, Pantnagar,
Uttarakhand, India
Babita Joshi
Ph.D Student, Dept. of Plant Physiology,
College of Basic Sciences and Humanities
GB Pant University of Agriculture and Technology, Pantnagar
Uttarakhand, India

Page | 113
Page | 114
 Chapter - 9
Herbicide Resistance: A Threat to Herbicide Utility and
Sustainability
Sudershan Mishra, Dr. S.K. Guru, Nitin Kumar, Prinsa Ramola, Babita Joshi

Appearance of herbicide resistant weeds is an upfront threat to utility and

sustainability of cropping in general and herbicides in particular. A plant is
attributed resistant to a herbicide if it is able to survive a normally lethal dose
of that herbicide. The resistance can be grouped as cross resistance
(resistance against many herbicides of the same class) or multiple resistance
(resistance against herbicides belonging to different groups). The various
factors that stimulate herbicide resistance may be weed characteristics,
herbicide characteristics and faulty cultural practices prevalent at the farm
i.e. operational factors. However bottom-line is that a weed becomes
resistant to herbicides due to lack of rotation of the herbicides and a long
residue period of certain herbicides. The evolution of herbicide resistance is
gradual and may be due to limiting out phenomenon or sequence change
phenomenon. Limiting out phenomenon involves modification in
physiological and/or biochemical mechanism of action of herbicides
underpinned by morphological adaptations. In case of sequence change
phenomenon one or more point mutations may lead to altercations in original
protein product to which herbicide originally bounded with and as a result of
non-binding of the herbicide to its target protein the weed biotype becomes
resistant. Also an increasing number of weeds are becoming resistant to
herbicides due to their enhanced metabolic capacity to detoxify herbicides.
Another alarming face is the prevalent use of herbicides at a dose lower than
recommended for the area. Lower doses enhance the occurrence of herbicide
resistance by a multitude of mechanisms. However there are some very basic
tweaks that are required in the current operating cultural practices to mitigate
this problem of herbicide resistance. This review is an in-depth discussion of
various mechanisms of herbicide resistance, how and when they arose,
quantification of prevalent herbicide resistance and how it can be managed.
The review also provides a bird’s eye view on novel mechanisms of soil
active pre-emergent herbicides and the very recent report of deletion
mutation conferring herbicide resistance.

Page | 115
Keywords: Herbicide Resistance. Mechanism of action. Mutation. Weeds.
Crops.
Introduction
Weeds are one of the major biological constraints that limit the
productivity. Weed-crop competition is very high for natural as well as
applied resources which reduces the quantity as well as quality of
agricultural productivity [1]. If quantitatively expressed the loss due to weeds
averages around 31.5% (22.7% in rabi and 36.5% in kharif), add to this the
environmental hazards it causes [2]. Among the different management
techniques to manage weeds chemical management (use of herbicides) has
been most popular and effective throughout the past decades. A range of
herbicides belonging to different chemical groups and having different
modes of action have been in widespread use to manage weeds effectively.
However at the same time prolonged use of herbicides have resulted in
certain weeds getting resistant to them. As of today herbicide resistance
stands as a global threat to sustainability of the food production with
hundreds of biotypes of weeds resistant to commonly applied herbicides
found throughout the world and the list is increasing day by day. Herbicide
tolerance is the inherent ability of a species to survive and reproduce
following a herbicide treatment while herbicide resistance is the inability of
a herbicide to effectively control a weed species that was previously
controlled by the same herbicide. Technically speaking Herbicide Resistance
may be defined as the inherited ability of a weed or crop biotype to survive
and reproduce following treatment with a dose of herbicide to which the
original population was susceptible [3]. Although it is not a very new concept,
in fact reports of resistance of wild carrot biotype to 2-4-D came as early as
1950 [4] while the first confirmed report of triazine resistance in common
groundsel (Senecio vulgaris) was reported in 1968 [5]. But what is alarming is
the rate at which the magnitude of resistance has gone up worldwide. At
least one weed species has emerged resistant to herbicide in each country of
the world where herbicide is used as a farm input. The resistance to 19
classes of herbicides has been reported in 330 biotypes of 189 species (13
dicots and 76 monocots) worldwide [6]. Continuous and intensive use of
similar herbicides on related crops/cropping systems puts heavy selection
pressure and as a result more and more resistant biotypes are selected with
each application. This leads to accumulation of resistant biotypes within the
community. Gradually this resistance to singular herbicide or group of
herbicides transforms to multiple resistance across one type of herbicide
posing an even bigger threat to crop production systems. The list of most

Page | 116
important herbicide resistant weeds includes Rigid ryegrass (Lolium
rigidum), Common waterhemp (Amaranthus redis), waterhemp (A.
retroflexus), ragweed (Ambrosia trifida), hairy fleabane (Conyza
bonariensis), Johnson’s grass (Sorghum halapense), wild oat (Avena fatua),
Little seed canary grass (Phalaris minor) [7]. The preferred method of
confirming herbicide resistant weeds is to conduct whole plant dose response
experiments on resistant and susceptible biotypes of same species under
green house or growth chamber conditions. Resistant weed population is a
serious constraint because it develops way faster (3-5 years only) than the
time required to develop, test and register a new weed killing chemical (8-
10) years that meets the current environmental and health regulatory
standards.
Factors Influencing Resistance Development
Herbicide resistance is an evolutionary and ecological process.[8] The
dynamics of this process are influenced by 1)weed characteristics which
further include the morphological and genetic factors associated with the
weed 2) herbicide characteristics which further includes mode or site of
action of herbicide and 3) finally the operational factors i.e. the prevalent
farm practices.[4]
Characteristics of Weed-
Morphological
1. Seed Factors-Enhanced seed production and low dormancy of seeds
leads to rapid turnover of weed seed bank. From the germinating
lot, susceptible biotypes get killed faster in presence of herbicide
and the leftover resistant ones though few in number will reproduce
and live better off the abundant resources now available to them due
to killing of susceptible ones. This process helps in efficient carry
forwarding of the resistant trait [9].
2. Mating system-Cross pollination leads to rapid spread of the
resistant trait as compared to self-pollination.
3. Dispersal of seed and/0r pollen-Distance of migration of seed or
pollen is the basic factor determining the evolutionary pace of
herbicide development.
4. Growth tendency-Annual weeds are more prone to resistance
development than biennials or perennials.

Page | 117
Genetic Factors
Important genetic factors include 1) intrinsic or initial frequency of
resistance genes in the population 2) the pattern of inheritance- whether the
resistance is dominant or recessive and 3) the fitness cost. fitness cost refers
to the selective advantage or disadvantage conferred by presence or absence
of resistant alleles.
Characteristics of Herbicides
1. Hyper-Efficacy-a single application of a highly effective herbicide
can eradicate 90-95% of susceptible population. Hence resistant
biotypes thrive better to stand fit in the field [10]
2. Residue period- Longer residue time causes selection pressure to
prevails for a longer time giving competition free growth autonomy
to resistant biotypes to flourish and reproduce [5].
3. No. of sites of action- resistance develops easily for herbicides with
a singular site of action
4. Susceptibility to metabolism-herbicides prone to enhanced
metabolism in the weeds easily develop biotypes resistant to them
[11]
.
Operational Factors
1. Cropping system-diversity of cropping system is inversely
proportional to rate of evolution of herbicide resistance
2. Rate of application of herbicide- application of lower than
recommended doses of herbicides leads to selection of minor traits
for resistance and their accumulation through cross pollination.
3. Frequency of application of herbicide- application of similar inputs
year after year leads to development of resistant biotypes
4. Tillage practices-reduced or conservation tillage leads to lesser
turnover of weed seed bank and lesser germination of weed seeds.
Thus selection for resistant traits could be minimized.
Mechanism of Herbicide Resistance
The various mechanisms of herbicide resistance can be grouped into
1. Limiting out phenomenon
2. Sequence change phenomenon
In any given herbicide resistant biotype the resistance may be due to any

Page | 118
one of the above stated phenomenon or due to simultaneous occurrence of
both of them.
Limiting out phenomenon is also called as non-target site resistance. In
this case resistance is developed by limiting the access of toxic molecule so
that it no longer accumulates in right lethal amounts at right p[point of
action. This can be achieved due to
1. Morphological mechanisms-overproduction of waxes, reduced leaf area,
extraordinarily increased waxy coating on cuticle, increased trichome
density and reduced foliage number are some of the morphological
changes that reduce herbicide access to sensitive regions
2. Physiological mechanisms-differential translocation also helps in
limiting out building up of toxic concentration at sensitive places. Also
certain lipophilic herbicides may get sequestrated into lipid rich glands
or oil bodies which limit their access [12, 13].
3. Biochemical mechanisms-Most of the biochemical mechanisms target at
enhanced herbicide metabolism and hence is also termed as metabolic
resistance. It can be endowed by increased activity of endogenous
cytochrome P450 monooxygenases (CytP450s), glucosyl transferases
(GTs), glutathione-s-transferases (GSTs), and/or other enzyme systems
such as aryl acyl amidases that can metabolize herbicides [11].
Sequence Change Phenomenon
This is also called as target site resistance. Unlike limiting out
phenomenon it has no effect on the concentration of the herbicide. It
involves point mutation(s) in the genetic sequence responsible for the protein
product (to which the herbicide originally binded with) so that it is no longer
suitable for binding with the herbicide. In certain cases the mutations may
lead to overproduction of the protein product so that effect of herbicide with
its normal rate of application gets diluted. The extra amount of enzyme
produced in this case allows the plant to continue its normal metabolic
activities by overcoming the lethal effects.
Mechanism of Resistance to Some Important Herbicides
PS II Inhibitors
1. Chemical families-Triazines, Triazinones, Uracils, Nitriles,
Phenylureas, Pyridiazinones and benzothiadiazole.
2. Mechanism of action-they disrupt the electron transport chain in
susceptible plants. The plastoquinones (PQA & PQB) which are the

Page | 119
 electron acceptors in photosynthetic electron transport chain. These
are attached to specific niches in D1 and D2 protein so that the
electron moves from PQA to PQB. The herbicide acts as the non-
reducible analogue of PQB and attaches itself to D1 at Ser 264 and
Phe265 with H-bonds rendering the plastoquinones unavailable for
electron transport. This is because the herbicide molecule is non-
reducible and it doesn’t receive electron from PQA. Due to this
triplet chlorophyll and singlet oxygen accumulate start lipid
peroxidation and lethal membrane disruption
3. Mechanism of resistance- resistance to PS II inhibitors is due to
mutations in the psbA gene that encodes the D1 protein. Base pair
substitutions generate various mutant alleles in psbA gene that
confer resistance to different herbicides. For example triazine
resistance is conferred by Ser-264-Gly amino acid substitution
while Ser-264-Thr substitution enables resistance against triazine as
well as ureas. However in Lolium, the resistance mechanisms
exhibiting limiting out phenomenon are reported to be more
important [14].
4. Spread- currently 69 species have been reported to be resistant to
PS II inhibiting herbicides [5].
PS I Inhibitors
1. Chemical Family-Bipyridinium e.g. paraquat (1, 1-dimethyl-4,4’-
bipyridinium)- used as a non-selective herbicide.
2. Mechanism of action- paraquat acts by accepting electrons from
early acceptors of PS I and thus disrupts the electr4on transport
chain. This leads to accumulation of ROS (reactive oxygen species).
ROS causes membrane disruption and subsequently death of plants
[14]
.
3. Mechanism of resistance-two different mechanisms have been
proposed both of which are targeted at limiting the translocation of
herbicide
a. Adsorption to cellular components as in case of Conyza bonariensis
b. Sequestration-it is actively transported into membrane bound
storage organelles to limit its translocation as in case of Lolium
rigidum
4. Spread-tolerance to paraquat was first reported in Lolium perenne
followed by Amaranthus lividus, Bidens Pilosa, Eleusine indica and
Solanum nigrum. So far 28 weed species have evolved resistance to

Page | 120
 this herbicide [7].
ACCase Inhibitors
1. Chemical family-Aryloxyphenoxypropionate (FOPs),
Cyclohexanedione (DIMs), Phenylpyrazolins (DENs), e.g. diclofop-
methyl (FOP), Clethodim (DIM), Pinoxaden (DEN). These are used
for post emergence grass control in broad leaf crops.
2. Mechanism of action- Acetyl CoA Carboxylase (ACCase) catalyzes
ATP dependent carboxylation of Acetyl CoA to form Malonyl CoA
which is the first step in fatty acid biosynthesis. ACCase inhibiting
herbicides bind to a specific domain on the enzyme that is close to
the catalytic site of the enzyme. After binding, the herbicide
overlaps with the catalytic site leaving the enzyme non-functional.
Dicots have a resistant ACCase hence such herbicides are
particularly used to target grassy (monocot) weeds [14].
3. Mechanism of resistance-resistance to these herbicides has been
achieved through both the strategies. Under the sequence change
phenomenon or target site resistance, it has been achieved due to an
amino acid substitution in the carbonyl transferase domain of
ACCase gene. Under the limiting out phenomenon it has been
achieved via enhanced detoxification mediated by CytP450 Mono-
oxygenase. Also resistance has been enabled in some cases by
greater membrane recovery response [15].
4. Spread-Resistance to ACCase inhibitors has been widespread
especially in Lolium rigidum in Australia and in Lolium
multiflorum, Avena fatua and Setaria viridis in North America.
Other weed species resistant to this group include Digitaria
sanguinalis, Echinochloa crusgalli, and Echinochloa colona. More
recently there have been reports about resistance to ACCase
inhibitors in Phalaris minor as well. A total of 43 grassy weeds have
evolved resistance to this group of herbicides [7].
ALS Inhibitors
1. Chemical family-Imidazolines (e.g. Imazethapyr), Pyrimidinyl
thiobenzoates (e.g. bispyribac-sodium), Sulfonyl ureas (e.g.
chlorsulfuron, metsulfuron-methyl), Troazolopyrimidines (e.g.
Diclosulam). Used for selective post emergence weed control.
2. Mechanism of action-These herbicides inhibit enzymes
Acetohydroxyacid synthase (AHAS) and/or Acetolactose synthase

Page | 121
 (ALS). AHAS/ALS is the first enzyme common to biosynthesis of
branched chain amino acids (leucine, valine and isoleucine). This
blockage starves the plant of these amino acids resulting in their death
[16]
.
3. Mechanism of resistance- different weed biotypes are able to resist
AHAS/ALS inhibitors by both target site as well as non-target site
mechanisms. While non-target site mechanism is due to rapid metabolic
inactivation by certain mixed function oxygenases, the target site
mechanism is due to a point mutation proline-179-histidine. This
substitution decreases the sensitivity of ALS/AHAS towards the
herbicide thus allowing the plant to survive the lethality [17].
4. Spread-initially it was reported in Lactuca serriola but it is also found in
Amaranthus spp. Conyza spp. Lolium spp. Avena fatua and Eleusine
indica. So far 127 weed species have evolved resistance to this group of
herbicides, highest for any one particular mode of action group [7].
Resistance to ESPS Inhibiting Herbicides and the Curious Case of
Glyphosate Resistance
1. Chemical family-derivatives of glycines e.g. glyphosate used as
non-selective post emergence herbicide in case of glyphosate
resistant transgenics
2. Mechanism of action- glyphosate inhibits 5-enolpyruvylshikimate-
3-phosphosate synthase (ESPS) which is the primary enzyme
responsible for synthesis of aromatic amino acids (via the shikimate
pathway) and certain secondary aromatic products like amines,
lignins and phytoalexins etc. The herbicide primarily inhibits
binding of phosphoenolpyruvate (PEP) TO ESPS. PEP is one of the
initial intermediate of the pathway. In the absence of aromatic
amino acids and/or their secondary products the plant is unable to
complete its viable life cycle.
3. Development of glyphosate resistant crops-2 kinds of ESPS are
known class I ESPS which is very sensitive (inhibited at micro
molar concentrations) and class II ESPS [18] which is relatively less
sensitive and is inhibited at mill molar concentrations. Initially
research in this area started with glycine-97-alanine substitutions
but these were not commercialized as the mutations increased the
Km value for PEP while conferring resistance to glyphosate [19]. A
double mutation threonine-97-isoleucine and proline-101-serine
was introduced into corn to produce first stable glyphosate resistant

Page | 122
 corn which is commercially even today. Glyphosate resistant
transgenics were produced in cotton, soybean and canola using
ESPS gene of Agrobacterium strain CP4. This enzyme had an
alanine at 100th position whose methyl group disallows binding of
herbicide to enzyme by providing steric hindrance to oxygen atoms
of glyphosate phosphonate group [20].
4. Mechanism of resistance-3 mechanisms of resistance towards
glyphosate have been elucidated. Following is a brief discussion
towards each one of them
a. Sequence change phenomenon or target site resistance- first
resistant biotype with this mechanism was reported in 2002 by Lee
& Nigin. Weeds become resistant either due to a Pro-101-Ser or
Pro-101-Thr point mutations, both of which reduce the affinity of
ESPS for glyphosate binding. However the same mutation
decreases the ESPS affinity for PEP (its original substrate). But the
clear mechanism of how weed deals with this fitness cost is not
studied yet [21, 22].
b. Amplified expression of ESPS- first glyphosate resistant biotype of
palmer amaranth (Amaranthus palmeri wats) was reported in 2004.
It has been reported that amplification as high as 77 more copies of
ESPS gene, 35 fold higher expression of ESPS mRNA and
approximately 20 fold higher expression of ESPS enzyme in certain
cases. A greater amount of enzyme has a dilution effect on the
herbicide and leads to survival of the weed biotype [23, 24].
c. Limiting out phenomenon-differential translocation is the most
common and most effective resistance mechanism to glyphosate
exhibited by plants and it can be easily inferred as well. This is
because shikimate pathway operates at apical portion and
glyphosate needs to be translocated to growing points via phloem.
Phloem mobility is due to unique combination of 3 acidic and 1
basic functional group on the herbicide. Any change that inhibits
this zwitter ion characteristics of herbicide or source to sink phloem
movement of sucrose will endow resistance to weed biotype. To
date no weed is known to show resistance to glyphosate due to
altered metabolism [25, 26].
5. Spread- as a herbicide glyphosate is being used since 1974, but the
first case was reported in 1994. It can be observed that resistance
evolution has been slow through the previous decades but now it is
increasing at an alarming rate. 16 weed species in 14 different

Page | 123
 countries have been reported to be resistant to glyphosate. Chief of
them are Eleusine indica, Lolium rigidum, Lolium perenne,
Amaranthus palmeri, Conyza spp [7].
Resistance to Microtubule Assembly Inhibitors
1. Chemical family-dinitroanillines (e.g. pendimethalin), benzoic acids
(e.g. DCPA), benzamide (e.g. proxamide), pyridines (e.g.
Thiazopyr). Used for pre-emergence grass and broad leaf weed
control.
2. Mechanism of action-these herbicides generally target germinating
weed seeds where they prevent dimerization of tubulin subunits
thus inhibiting cell division and transport.
3. Mechanism of resistance-at genetic level certain point mutations
such as thr-239-leu can confer high level of resistance while others
such as met-218-thr can provide a low level of resistance. A
characteristic feature of these changes is that these are encoded by
recessive single nuclear gene. Hence only homozygous recessive
individuals show the resistant trait. This trait is advantageous for us
as heterozygotes would get killed at normal herbicide dose resulting
in very slow resistance evolution towards such herbicides.
4. Spread- First reported in Eleusine indica in 1998 but since then it
has been reported in only 10 weed species up to now.
Resistance to Protoporphyrinogen Oxidase (PPO) Inhibitors
1. Chemical groups-diphenylether (e.g. oxyfluorfen), oxadiazole (e.g.
oxadiazone), triazolinone (carfentrazone-ethyl). Used for spot
application as these are highly effective contact herbicides.
2. Mechanism of action-the enzyme (PPO) converts
protoporphyrinogen IX into porphyrinogen IX. The latter is a
common precursor for both heme and chlorophyll. The enzyme has
a mitochondrial (PPO2) and chloroplastic (PPO1) form encoded by
genes PPX2 and PPX1 respectively. In the presence of herbicide
PPO is inactivated and plant dies.
3. Mechanism of resistance- the resistance mechanism is unique and is
the only case of amino acid deletion conferring herbicide resistance.
A 3bp codon deletion of glycine-210 in both PPX1 and PPX2
results in a resistant biotype [27].
4. Spread- reported in very few weed species particularly in

Page | 124
 Amaranthus tuberculates. Resistance to carotenoid inhibitors has
been reported in Hydrilla verticillata and Raphanus raphanistrum in
Australia. The low level of occurrence of resistance in such cases
makes these attractive herbicide tools for the coming decades
A Brief Discussion on Isoproturon Resistance in Phalaris Minor
Isoproturon resistance in P.minor (Little seed canary grass) is one of the
most serious cases of herbicide resistance that has surfaced in recent times
for the world in general and India in particular. The first case of isoproturon
resistance was reported from India in 1995 [6] where it was concluded that
continuous use of isoproturon coupled with mono-cropping of rice –wheat
for over a decade led to evolution of resistance to the herbicide. Although
initially reported from Punjab and Haryana the problem is now widespread
throughout wheat growing areas of India.
Resistance mechanisms have been reported to be both due to target site
mutations and due to enhanced metabolism. What is even more problematic
is the fact that over the years P.minor biotypes have developed resistance to
a range of herbicides with different mechanisms of action such as ALS
inhibitors, ACCase inhibitors and even tank mixes of certain herbicides like
mesosulfuron + idodosulfuron [28]. Although many integrated approaches
with focused attention on zero tillage are being popularized but still P.minor
poses a significant threat to wheat growers in India [29].
Management of Herbicide Resistance
Unique situations present differential selection pressures that lead to
development of herbicide resistance. Hence a singular strategy cannot be
applied for management of resistance. However multiple control strategies
available for herbicide management can be broadly grouped under the
following heads
1. Managing Soil Load- Judicious use of tillage has been proved to be
helpful in managing herbicide resistance in both conservation
tillage as well as reduced tillage systems. It basically helps by
allowing a greater weed kill achieved through disturbance of soil.
Targeted tillage integrated with cultural practices such as organic
mulches and soil solarization provides a good chance of complete
removal of biotype.[30]
2. Managing Crop Load- Diversity in the crop rotation automatically
mandates diversity in herbicide use thus reducing the chances of
evolution of herbicide resistance. This also reduces the chances of

Page | 125
 establishment of resistant biotypes against a singular herbicide
which otherwise is very high in mono-cropping as same weed seed
bank gets cycled again and again
3. Managing Herbicide Load- this can be done using three different
strategies
a. Reducing dose strategy- alternating high doses with low doses helps
to reduce both monogenic as well as polygenic resistance from the
population
b. Combination mix strategy- Using a combination of herbicides
reduces risk of development of resistance as there is less exposure
against a single herbicide.
c. Allelopathic cultivar development- Allelopathy refers to
phenomenon of secretion of certain chemicals from a plant that
inhibits growth of other plants nearby it. A crop when itself is able
to manage weed due to its allelopathic effect, it can directly reduce
the herbicide load
Conclusion
It can be easily agreed upon that no herbicide is immune to evolution of
herbicide resistance and there is no silver bullet as every herbicide has its
own advantages and disadvantages. Resistance to herbicides has been
increasing at an alarming rate since the last four decades. The screening
strategies for herbicide resistance has to grow at the same pace as well and a
diverse number of physiological and biochemical screening methods with
quick results need to be developed to catch the resistance at its headway and
manage it. Awareness for herbicide stewardship particularly for non-
selective herbicides being used on transgenic crops need to be enhanced.
Herbicide resistance is a threat to modern herbicide technology with its
vastly negative bearing on food production worldwide. More use of
molecular tools is needed in this field to reduce the frequency of this
phenomenon by early screening and disposal.
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