IT OCCURS BECAUSE THERE IS VARIATION IN WEED POPULATIONS AND A SELECTIVE PRESSURE (THE HERBICIDE ) THAT FAVOURS CERTAIN INDIVIDUALS

1. DEVELOPMENT OF HERBICIDE
RESISTANCE --- IN WEEDS AND ITS
MANAGEMENT.
Presented by-
Miss Susmita Das
Department of Agronomy,
CAU, Imphal

2. PARTHENIUM HYSTEROPHORUS- A WEED OF
NATIONAL IMPORTANCE

3. HERBICIDE AND ITS HISTORY
 ANY CHEMICAL USED TO KILL WEED OR ANY
UNWANTED PLANTS IN THE CROP FIELD IS CALLED
WEEDICIDE OR HERBICIDE.
 THE USE OF CHEMICAL WEED MANAGEMENT DATES
BACK TO THE LATE 19 th CENTURY WHEN COPPER
SULPHATE , A CONSTITUENT OF BORDEUX MIXTURES
WAS FOUND TO KILL SOME WEEDS PRESENT BETWEEN
THE VINES.
 IN ANCIENT TIMES WEED MANAGEMENT INVOLVES
HAND – WEEDING METHODS AND ANIMAL DRAWN
CULTIVATION SYSTEMS.
 MAJOR ADVANCES IN CHEMICAL WEED
MANANAGEMENT WAS FROM THE PERIOD OF 1941
TO 1968 WHEN 2,4-D WAS DEVELOPED IN AMERICA
IN 1941.

4. WHAT IS HERBICIDE RESISTANCE ?
 RESISTANCE IS THE NATURALLY OCCURING HERITABLE
ABILITY OF SOME WEED BIOTYPES WITHIN A POPULATION TO
SURVIVE A HERBICIDE TREATMENT THAT WOULD , UNDER
NORMAL CONDITIONS OF USE , EFFECTIVELY CONTROL THAT
WEED POPULATION.
 SELECTION OF RESISTANT BIOTYPES MAY EVENTUALLY
RESULT IN CONTROL FAILURES.
 THE FIRST REPORT OF HERBICIDE RESISTANCE IS RESISTANCE
OF TRIAZINE HERBICIDES IN SENECIO VULGARIS BY RYAN (1970 )
WHICH IS THE MOST COMMON TYPE OF RESISTANCE
WORLDWIDE.
 SOME NEW WEEDICIDE GROUP ARE ALSO RAPIDLY
EVOLVING RESISTANCE.

5. CHART SHOWING THE NUMBER OF WEED SPECIES WITH
HERBICIDE-RESISTANT POPULATIONS
CHART SHOWING THE NUMBER OF WEED SPECIES WITH HERBICIDE
RESISTANT POPULATIONS IN SOME OF THE COUNTRIES
COUNTRY NO COUNTRY NO COUNTRY NO COUNTRY NO
INDIA 1 AUSTRALIA 22 GERMANY 15 INDONESIA 2
USA 49 CANADA 22 SWITZERLAND 13 MEXICO 2
FRANCE 24 ISRAEL 18 BELGIUM 11 KENYA 2
SPAIN 24 UK 16 CHINA 4 PHILLIPINES 1

6. RESISTANT HERBICIDE- GROUPS

TRIAZINES
 43 DICOTYLEDONOUS AND 18
MONOCOTYLEDONOUS WEED SPECIES HAVE
DEVELOPED RESISTANCE TO THIS HERBICIDE.
 MOST COMMON TRIAZINE-RESISTANT
POPULATIONS ARE Chenopodium album (16
countries ), Amaranthus retroflexus(10
countries), Senecio vulgaris (10 countries) ,
and Solanum nigrum (9 countries ).
 IT HAS BEEN ESTIMATED THAT TRIAZINE-
RESISTANT WEEDS INFEST MORE THAN 3
MILLION HAC. WORLD WIDE.
ALS
INHIBITORS
 HERBICIDE THAT INHIBIT ACETOLACTATE SYNTHASE
ENZYME ACCOUNTS FOR 17 % OF THE GLOBAL MARKET,
THEIR WIDESPREAD USAGE AND EASE
HAS DEVELOP RESISTANCE IN 26 DICOTYLEDONS AND 7
MONOCOTYLEDON SPECIES.
 DURING 1997 , THERE WERE 13 WEED SPECIES WITH ALS-
RESISTANT POPULATIONS IN USA, 9 IN AUSTRALIA, 5 IN
CANADA, AND 5 IN ISRAEL.

7. RESISTANT HERBICIDE-GROUPS

PHENYLUREAS AND
PHENYLAMIDES
 14 WEED SPECIES AND 2 WEED SPECIES HAVE DEVELOPED RESISTANT TO
PHENYLUREAS AND PROPANIL ( an amide ).
 THE FIRST PHENYLUREA RESISTANT WEED WAS Alopecurus
myosuroides FROM UK IN 1982.
 SOME OF THESE RESISTANT POPULATIONS CAN CAUSE SERIOUS
PROBLEMS DUE TO CROSS-RESISTANCE TO ALTERNATIVE HERBICIDES
OF DIFFERENT MODES OF ACTION.
 WIDESPREAD OCCURENCE OF ISOPROTURON RESISTANCE IN
PHALARIS MINOR IN INDIA IS CURRENTLY AFFECTING WHEAT
PRODUCTION IN AFFECTED AREAS.
BIPYRIDILIUMS
 PARAQUAT AND DIQUAT BELONGING TO THESE GROUP ARE NON-
SELECTIVE, NON-PERSISTENT,AND FAST ACTING POST-EMERGENCE
HERBICIDES, THESE ARE WIDELY USED IN ORCHARDS AND
PLANTATIONS CROPS.
 THERE ARE 20 DICOTYLEDON AND 7 MONOCOTYLEDON SPECIES
RESISANT TO BIPYRIDYL HERBICIDES.

8. RESISTANT HERBICIDE-GROUPS
SYNTHETIC
AUXINS
 CONSIDERING THE EXTENSIVE USE OF THIS HERBICIDES
LIKE 2,4-D AND MCPA FOR OVER 50 YEARS, FEW
WEEDS HAVE DEVELOPED RESISTANCE.
 SOME HABITATS ARE SUGARCANE FIELDS IN HAWAII,
PASTURES IN NEW ZEALAND, AND RICE CROPS IN RICE.
 IN TOTAL 14 WEED SPECIES HAVE DEVELOPED
RESISTANCE TO THIS HERBICIDES.

9. RESISTANT HERBICIDE GROUPS

ACCase INHIBITORS
 Acetyl –Coenzyme A Carboxylase ( ACCase inhibitors )
WERE 1st
RELEASED IN THE LATE 1970s.
 THEY PROVIDE EXCELLENT CONTROL OF GRASS WEEDS IN
BOTH CEREALS AND BROADLEAVED CROPS.
 WIDELY ACCECPTABLE AND CONTAINS 5% OF GLOBAL
HERBICIDE SALES.
 WEED SPECIES LIKE LOLIUM SPP, AVENA SPP AND
PHALARIS SPP ETC HAVE DEVELOPED RESISTANCE
TOWARDS THIS GROUP.
GLYPHOSATE
 IT IS CONSIDERED AS A LOW RISK HERBICIDE FOR RESISTANT
DEVELOPMENT.
 ITS MODE OF ACTION, CHEMICAL STRUCTURE , LIMITED
METABOLISM IN PLANTS, USE PATTERN AND LACK OF
RESIDUAL ACTIVITY , ARE REASONS WHY THIS HERBICIDE IS
UNLIKELY TO SELECT FOR RESISTANCE.
 LOLIUM RIGIDUM IS THE ONLY WEED WORLD WIDE TO HAVE
DEVELOPED RESISTANCE AGAINST GLYPHOSATE.

10. EVOLUTON OF HERBICIDE RESISTANCE- WHY AND
HOW IT OCCURS ?
 HERBICIDE RESISTANCE IS AN EVOLUTIONARY
PROCESS.
 IT OCCURS BECAUSE THERE IS VARIATION IN
WEED POPULATIONS AND A SELECTIVE
PRESSURE (THE HERBICIDE ) THAT FAVOURS
CERTAIN INDIVIDUALS .
 BY CONTROLLING THE VAST MAJORITY OF
INDIVIDUALS WITHIN A POPULATION , THE
HERBICIDE ACTS AS A STRONG SELECTION
PRESSURE THAT SELECTS FOR RESISTANT
TYPES.
 THE MAJOR FACTORS INFLUENCING THE
RESISTANCE ARE: 1) INTENSITY OF THE
SELECTION PRESSURE.

11. A. INTENSITY OF SELECTION PRESSURE
 IT IS A COMBINATION OF THE EFFICACY PROVIDED
BY THE HERBICIDE IN ANY GENERATION AND THE
NUMBER OF WEED GENERATIONS TARGETED BY
HERBICIDES.
 HERBICIDES ARE DESIGNED TO CAUSE HIGH
MORTALITY OF WEEDS, i.e THE SELECTION
PRESSURE IS DOMINATED BY THE NUMBER OF
WEED GENERATIONS, THE HERBICIDE IS USED
AGAINST.
 A GREATER PROPORTION OF THE EMERGING
WEED POPULATION ARE EXPOSED TO HERBICIDE
WITH EXTENSIVE SOIL ACTIVITY , INCREASING
THE INTENSITY OF SELECTION.
 IN RARE CASES, A SINGLE APPLICATION MAY

12. B . INITIAL FREQUENCYOF RESISTANT INDIVIDUALS
 EVOLUTION CAN ONLY OPERATE IF THERE IS
VARIATION WITHIN THE POPULATION FOR
CHARACTERISTICS AND IN HERBICIDE
RESISTANCE,VARIATION IN TOLERANCE TO THE
HERBICIDE IS REQUIRED.
 THE INITIAL FREQUENCY OF INDIVIDUALS
RESISTANT TO A HERBICIDE IS USUALLY VERY
LOW . VALUES OF 10-6 (i.e 1 resistant individual in
every million ) are commonly assumed.
 IT CAN BE DETERMINE BY THE MUTATION
FREQUENCY AT THAT GENE, THE FITNESS OF THE
RESISTANT ALLELE COMPARED TO
SUSCEPTIBLES, AND THE LEVEL OF DOMINANCE

13.  THIS CAN BE DESCRIBED BY THE EQUATION: q e =
u/h.s where ‘q e’ is the equilibrium frequency of
resistant individuals in a population, ‘u’ is the mutation
frequency at that locus, ‘h’ is the degree of dominance
of the resistant allele, and ‘s’ is the fitness differential of
the resistance allele compared to the susceptible allele.
 DUE TO THE HIGH INTENSITY OF SELECTION BY
THE HERBICIDE, FITNESS OF THE RESISTANT
ALLELE HAS LITTLE IMPACT ON THE SPEED OF
SELECTION DURING YEARS WHEN THE
HERBICIDE IS USED.

14. C. IMPACT OF WEED BIOLOGY ON EVOLUTION OF
RESISTANCE
 THE BIOLOGY OF WEED SPECIES CAN INFLUENCE
THE DEVELOPMENT OF RESISTANCE.
 RESISTANCE IS MOST LIKELY TO APPEAR IN
WIDESPREAD WEED SPECIES THAT OCCUR IN
HIGH NUMBERS.
 THIS MAXIMISES THE OPPURTUNITIES FOR
SELECTING RARE RESISTANT INDIVIDUALS.
 ALSO, RESISTANCE WILL OCCUR MORE SLOWLY
IN A SPECIES WITH A PERSISTENT SEED BANK IN
THE SOIL.

15. MECHANISMS OF
RESISTANCE
 HERBICIDE APPLICATION WILL SELECT ANY
TRAIT THAT GIVES A PLANT THE ABILITY TO
SURVIVE .
 THERE ARE THREE BROAD TYPES OF
BIOCHEMICAL CHANGES THAT CAN ENDOW
RESISTANCE TO HERBICIDES.
 THEY ARE --
1. TARGET SITE –BASED RESISTANCE
2. RESISTANCE DUE TO INCREASED HERBICIDE
DETOXIFICATION.
3. RESISTANCE DUE TO SEQUESTRATION OF
HERBICIDE.
4. CROSS-RESISTANCE.
5. MULTIPLE RESISTANCE.

16. 1. TARGET SITE- BASED RESISTANCE
 GENERALLY, THIS RESISTANCE RESULTS FROM A
SINGLE NUCLEOTIDE CHANGE ( a mutation ) IN THE
GENE ENCODING THE PROTEIN TO WHICH THE
HERBICIDE NORMALLY BINDS.
 EX-RESISTANCE TO THE TRIAZINE HERBICIDES,
SUCH AS ATRAZINE AND SIMAZINE ARE DUE TO
CHANGE IN THE TARGET SITE.
 TRIAZINE HERBICIDES ARE POTENT INHIBITORS OF
PHOTOSYNTHESIS AT PHOTOSYSTEM II (PS II ). THEY
BIND TO THE PLASTOQUINONE(QB) BINDING SITE ON
THE DI Protein AND INHIBITS ELECTRON FLOW.
 RESISTANCE TO TRIAZINE HERBICIDE ARE THE
RESULT OF A SINGLE AMINO ACID CHANGE WITHIN
THE DI PROTEIN.
 THIS REDUCES THE ABILITY OF TRIAZINES TO
INTERACT WITH PS II BY OVER THOUSAND FOLD

17. 2. RESISTANCE DUE TO INCREASED HERBICIDE
DETOXIFICATION
 In weed population , the herbicide is detoxified at a rate sufficiently rapid
that the plant is not killed, however plants frequently suffer an early
check to growth.
 Three enzymatic systems are known to be involved-----
a) Resistance to atrazine in some population of Abutilon
theophrasti is due to increased activity of specific
glutathione-S-transferases that detoxify atrazine. These
populations are only resistant to triazine herbicides.
b) Resistance to propanil in populations of Echinochloa
colona is due to increased activity of an Aryl
acylamidase that detoxifies propanil.
c) Increased herbicide metabolism due to enzyme
Cytochrome P450 monooxygenases causes resistance
to inhibitors of AACase,
ALS, and PSII in a number of grass weed species.
d) For ex- Isoproturon is metabolised by two different
types of Cytochrome p450 reactions in Phalaris minor.

18. HERBICIDE.
 The third way of resistance is through Sequestration of
the herbicide away from its active sites in the plants.
 Sequestration may occur at the cell level or at the organ
level.
 Effective Control of many Herbicide is achieved only if
sufficient herbicide reaches the target enzymes at
growing points (meristems ) in the plants or otherwise
the plant will survive.
 For ex- Paraquat resistance in Hordeum glaucum
and Glyphosate resistance in Lolium rigidum

19. 4. CROSS- RESISTANCE
 IT IS WHERE A WEED BIOTYPE IS RESISTANT
TO TWO OR MORE HERBICIDES DUE TO
PRESENCE OF A SINGLE RESISTANCE
MECHANISM.
 THEY ARE OF TWO TYPES-
---TARGET SITE BASED CROSS RESISTANCE
---METABOLISM BASED CROSS RESISTANCE
 FOR EX- THE 4 CLASSES OF CHEMISTRY THAT
INHIBIT ALS SHARE FEW SIMILARLITIES AND
OBIVIOUSLY BIND DIFFERENTLY TO THE ALS
ENZYME.
THE MUTATION AT ALANINE 122 RESULTS IN
RESISTANCE TO THE IMIDAZOLINONE AND ,
WHEREAS THE MUTATION AT TRYPTOPHAN 591
RESULTS IN RESISTANCE TO ALL 4 CLASSES OF

20. 5. MULTIPLE RESISTANCE
.
 IT IS A SITUATION WHERE MULTIPLE
MECHANISMS CONTRIBUTE TO HERBICIDE
RESISTANCE .
 IN A WEED POPULATION , IT IS POSSIBLE THAT
MORE THAN ONE TYPE OF RESISTANCE IS
PRESENT, THEY MAY CROSS WITH EACH OTHER
PRODUCING SOME PROGENY WITH BOTH
RESISTANCE MECHANISMS.
 FOR EX-One L. rigidum population in australia has
resistance due to mutations in two different herbicide
target sites as well as increased metabolism of
herbicides from atleast 5 different herbicide

21. 6. NEGATIVE CROSS-RESISTANCE
 A HERBICIDE- RESISTANT WEED POPULATION IS
MORE SUSCEPTIBLE TO OTHER HERBICIDE
THAN WILD TYPE BECAUSE THE RESISTANT
POPULATION HAS SIGNIFICANTLY LOWER
FITNESS THAN WILD TYPE.
 SOMETIMES THIS IS DUE TO A CHANGE IN THE
HERBICIDE TARGET ENZYME THAT MAKES THE
ENZYME MORE SUSCEPTIBLE TO OTHER
HERBICIDES THAT INHIBIT THE SAME ENZYME.
THIS LATTER SITUATION IS CALLED NEGATIVE
CROSS-RESISTANCE.
 FOR EX--- TRIAZINE RESISTANT PSII REACTIONS
ARE MORE SUSCEPTIBLE TO DINOSEB, AN
INHIBITOR OF PSII WITH DIFFERENT CHEMISTRY

22. MANAGEMENT OF RESISTANT WEEDS
 INTEGRATED WEED MANAGEMENT (IWM ) INCLUDES
PHYSICAL , CHEMICAL , AND BIOLOGICAL METHODS
SUCH AS ---
 CROP ROTATIONS.
CULTURAL PRACTICES LIKE STUBBLE BURNING,
DELAYED SOWING TO MAXIMISE PRE- SOWING
WEED KILL, AUTUMN CULTIVATION, INCREASING
CROP DENSITY FOR WEED SUPRESSION,
SELECTING CROP GENOTYPES WITH SUPERIOR
WEED SUPRESSION CAPACITY ETC.
ALTERNATIVE HERBICIDES.

23. CONCLUSION
 The evolution of herbicide resistance in weed species
has provided an additional constraint to agricultural
production.
 Herbicide resistance is the result of relaince on a single,
highly efficacious weed control tool like chemicals.
 Weeds can develop resistance to herbicides through a
variety of mechanism, target site changes and
increased herbicide detoxification are common.
 No Herbicide is likely to be immune from resistance.
 For future , the entire agri-industry is to develop frame-
works that enable early detection of resistance on farms
and to develop and implement alternative strategies that
extend the useful life of herbicides and enable farm
profitability to be maintained.

24. BIBLIOGRAPHY
 RECENT ADVANCES IN AGRONOMY, Ch- Development Of
Herbicide Resistance In Weeds and its Management. Page-337-355.
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