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PRESENTED TO
Dr. N.K. CHOUBEY
DEPARTMENT OF AGRONOMY
PRESENTED BY
SUBHASHREE MOHAPATRA
M.Sc. (Agri.), 1st year
DEPARTMENT OF AGRONOMY
ID. No. 2231070060
CONTENT
• INTRODUCTION
• RESISTANT WEED SURVEY AND
CURRENT SCENARIO IN THE WORLD
• DEFINITION OF HERBICIDE
RESISTANCE
• TYPES OF HERBICIDE RESISTANCE
• FACTORS AFFECTING RESISTANCE
DEVELOPMENT
• MECHANISM OF HERBICIDE
RESISTANCE
• RESISTANCE MECHANISM TO
HERBICIDE GROUPS
INTRODUCTION
Herbicide and Herbicide
Resistance:
• Any chemical used to kill weed or any unwanted plants in
the crop field is called herbicide.
• The use of chemical weed management dates back to the
late 19th century when Copper Sulphate , a constituent of
Bordeaux mixtures was found to kill some weeds.
• Common Groundsel (Senecio vulgaris) – Atrazine was
detected in Washington ( UAS ) in 1968 and was reported
by Ryan in 1970.This was first report of herbicide
resistance.
• In India, first case was Phalaris minor developed
resistance to isoproturon during 1992-93 reported by
Malik and Sing.
• Maximum numbers of cases of weed resistance to
DEFINITION OF HERBICIDE
RESISTANCE
• The inherent ability of plant / biotype to
survive and reproduce following exposure to
a dose of herbicide normally lethal to the
wild type
• In a plant it may naturally occur or may get
induced by such techniques as genetic
engineering or selection of variants
produced by tissue culture or mutagenesis.
EXAMPLES OF HERBICIDE RESISTANCE
HERBICIDE RESISTANT WEEDS
Propanil Echinochloa crusgali, Echinochloa
colona
Chlorosulfuron Lolium rigidum , Kochia scoparia
Sulfosulfuron Phalaris minor
2,4 -D Daucus carota , Commelina diffusa
Simazine Lolium rigidum
Isoproturon Phalaris minor, Cirsium arvense
Diclofop-methyl Lolium rigidum
RESISTANCE FACTOR
• Resistance factor (GR 50) – It is based on % inhibition in dry weight of the plant.
Resistance Factor =
GR 50 value of resistance population
GR 50 value of susceptible population
Q. If the dry matter of the resistant population of Phalaris minor to Isoproturon in wheat field is
estimated as 412kg where as susceptible population estimated as 238kg in 1hectare area.
Determine the resistance factor and state whether isoprotruron is recommendable or not?
Ans:- Dry wt. of resistant population = 412kg , Dry wt. of susceptible population = 238kg,
Resistance factor = 412/238 =1.73
Thus, the value of Resistance factor is >1, so isoprotruron is absolutely recommendable to
the field.
RESISTANCE WEED SURVEY AND CURRENT
SCENARIO IN THE WORLD
• The Survey of herbicide resistance weeds is a major tool for management.
• The purpose should be :- To monitor the occurrence of herbicide resistance weeds.
To access their economic impact all over the world.
• First world wide survey of herbicide resistant weeds was conducted by Homer Lebaron
in 1990 & 1991.
CHART SHOWING THE NUMBER OF WEED SPECIES
WITH HERBICIDE RESISTANCE GROUPS
COUNTRY WEED
BIOTYPES
GERMANY 19
CHINA 9
CANADA 44
UK 24
MEXICO 3
COUNTRY WEED
BIOTYPES
INDIA 3
FRANCE 32
USA 122
SPAIN 24
AUSTRALIA 51
TYPES OF HERBICIDE
RESISTANCE
1. Simple Resistance
2. Cross Resistance
3. Negative Cross resistance/
Collateral Sensitivity
4. Multiple Resistance
5. Reverse Resistance
6. Co- Resistance/ Compound
Resistance
SIMPLE RESISTANCE
• It is simply the resistance of a weed species due to its continuous exposure to an herbicide.
• In other words, it is resistance of one herbicide to one particular mechanism.
Complete/full resistance
• Resistance biotype are not at all affected by the herbicide used at the recommended dose.
• Its growth and reproduction (seed production) continue unabated and as usual even after that
herbicide application.
Partial resistance ( Rubin, 1991 )
• Resistance biotypes receive severe inhibition on their vegetative growth by the herbicide used
at the recommended dose. However, they continue to grow insufficiently and reach to
flowering and produce some seeds.
CROSS RESISTANCE
• It evolves when a weed species already resistance to a herbicide shows resistance to
other herbicides of the same chemical class to which it had never been exposed or it
shows resistance to two or more herbicides due to single resistance mechanism.
• Simply, resistance of two or more herbicides to single resistance mechanism.
• It is of two types – Target Site- based Cross – Resistance
Metabolic Cross Resistance
For e.g.:- Imazethapyr resistant Setaria faberi shows cross resistance to nicosulfuron.
Target Site – based Cross Resistance:-
• Resistance to two or more herbicides of similar or dissimilar chemical groups inhibiting the
same target site due to similar target site alteration.
• For e.g.: found in herbicides of triazines, triazinones,phenylureas,uracils.
Metabolic Cross Resistance :-
• Resistance to two or more herbicides of similar or dissimilar chemical groups or their toxic
metabolites due to similar rate of degradation of the herbicides.
• For e.g.:- Phalaris minor shows resistance to isoproturon.
Crop Weed With the use
of Herbicide
Cross
Resistance
Country /
Region
Wheat Phalaris minor Isoproturon Diclofop-p-methyl
Fenoxaprop-p-
ethyl
Clodinafop
propargyl
Sulfosulfuron
Punjab, Haryana
Punjab, Haryana
Punjab, Haryana
Punjab, Haryana
Wheat Alopecurus
myosuroides
Isoproturon Clodinafop
propargyl
UK
Crop Weed With the use
of Herbicide
Cross
Resistance
Country /
Region
Maize, Soybean Seteria faberi Nicosulfuron Imazethapyr USA
Rice Cyperus difformis Sulfonylureas Bispyribiac
sodium
Italy
Wheat Lolium rigidum Diclofop - p -
methyl
Chlorosulfuron Australia
Negative Cross-resistance/Collateral Sensitivity
• It refers to the mechanism by which an individual resistant to one herbicide or a
chemical family of herbicides shows higher or increased herbicides sensitivity to other
herbicides than its natural wild type susceptible population.
• This happens very frequently due to change in the target enzyme. The change makes
enzyme more vulnerable to other herbicides inhibiting the same enzyme.
• For example; the atrazine resistant biotype of Echinochloa crusgalli shows more
sensitivity to fluazifop-butyl and sethoxydim.
Multiple Resistance
• It is the resistance through which a weed species shows resistance to herbicides of different
chemical classes having different mode of action by two or more distinct resistance
mechanisms.
• Thus resistance to several herbicides resulting from two or more distinct resistance
mechanisms takes place in the same plant (more than one mutation).
• The classical example of multiple resistance is Lolium rigidum against various group of
herbicides.
• Multiple resistance was first reported in Lolium rigidum in Australia and Alopecurus
myosuroides in Europe.
• Alopecurus myosuroides developed resistance to chlortoluron in 1982 in U. K. and in 1983
in Germany.
Reverse Resistance
• It is a term used to describe a phenomenon or situation in which the weed biotype
resistant to a herbicide fall susceptible to the very herbicide if it is not used for a Period of
7-10 years, in stead some alternative herbicides used to kill the resistant population.
• It is believed to be a natural phenomenon that susceptible population becomes resistant
on repeated Exposure to a herbicide and it reverts back to be susceptible one if the very
herbicide is not used for sufficiently Long period.
Co-Resistance/Compound Resistance
• . Co-resistance is a term used to designate a resistance phenomenon in which a weed
develops resistance to both mixing partner herbicides of a mixture applied concurrently.
• This is a limitation of herbicide mixtures, which may seldom occur.
• This suggests that herbicide mixture also cannot completely rule out the development of
multiple resistance.
• Only example so far, Lolium rigidum developed resistance to amitrole and atrazine applied
to concurrently.
FACTORS AFFECTING
RESISTANCE
DEVELOPMENT
WEED FACTORS:
1. Initial frequency for resistance
development
2. Hypersensitivity of the susceptible
weed species to herbicide
3. Selection Pressure
4. Biological fitness
5. Weed Biology
6. Mode of inheritance of resistance
genes
H ER B IC ID E FA C TOR S
• Application of highly potent herbicides
• Specific mode of action with single
target Site
• Overdependence and Frequent
application of herbicides without
rotation
• Longer residual activity in soil
C R OPPIN G PR A C TIC ES
• Tillage
• Crop monoculture
MECHANISM OF
HERBICIDE RESISTANCE
Exclusionary mechanism of resistance
• Differential herbicide uptake
• Differential translocation
• Sequestration
• Enhanced metabolism/degradation
Target site mechanism of resistant
• Altered site of action/target site alteration
• Site of Over-production
Exclusionary mechanism of resistance
Exclusionary mechanism of resistance:
It refers to those mechanisms which exclude or take away herbicide molecules from the site of action in plants where they induce toxic
effect.
Differential herbicide uptake:
Herbicide resistance biotypes take up fewer amounts of herbicide molecules may be due to reduced leaf area,
Waxier leaves etc.
Differential translocation:
Less herbicide uptake result in its less translocation, that is, Lolium rigidum resistance to chlorsulfuron.
Sequestration and compartmentation:
It refers to the storing, accumulation and sequestration of herbicide in vacuoles, cells or tissues away from the
actual site of action of that herbicide and thus prevents the reaching of herbicide at site of action, e.g.
bipyridiliums( Paraquat)
Enhanced metabolism/ degradation:
• Quick degradation of herbicide into non – toxic metabolites into the plant before reaching to
the site of action.
• It is found in phenylureas (isoproturon,chloroturon), ‘fop’ , ‘prop’ and ‘dim’ herbicides,
bipyridiliums ( also sequestration) and triazines.
(Enhanced Metabolism) (Sequestration)
Target site mechanism of resistance
Altered site of action/ target site alteration :
• It is the alteration in the binding site of an
herbicide due to some genetic changes in
biotypes showing resistance, and this
herbicide molecule do not bind to the site of
action.
Site of overproduction:
• In this , site of action is produced in an
excess amount and so normal rate of
herbicide application can’t deactivate the total
enzyme produced.
Resistance Mechanism to Herbicide Groups
HERBICIDE RESISTANCE MECHANISM
Triazines • Resistance to PS II inhibitors.
• Target site alteration/ point mutation in
psbA gene.
• Enhanced degradation through glutathione
conjugation. (e.g., Abutilon theophrasti to
atrazine)
• Enhanced degradation through oxidization
of Herbicide. ( e.g., Simazine resistant
Lolium rigidum by cytochrome P-450
monooxygenase
Phenylureas (isoproturon, chloroturon ) • Enhanced metabolism – e.g., Phalaris
minor resistance to isoproturon through
de-alkylation and ring alkyl oxidation by
NADPH – cytochrome.
• Target site alteration – Phalaris minor
resistance to clodinafop
Paraquat • Resistance to PS-I inhibitors
• Detoxification of toxic products formed –
(e.g., conyza bonariensis)
• Rapid sequestration and
compartmentation (e.g., Hordeum
leporinum)
Dinitroanilines • Resistance to mitotic disruptions
• Target site alteration (e.g., Eleusine
indica)
Fop , prop and dim herbicides • Resistance to ACCase inhibitors.
• Target site alteration (Lolium rigidum
Resistance to diclofop- methyl.)
• Enhanced degradation ( e.g.:-
Alopecurus myosuroides)
• Overproduction of ACCase .
Chlorosulfuron • Resistance to ALS/AHAS inhibitors
• Target site alteration (e.g., Kochias
coparia)
• Enhanced degradation ( Lolium rigidum)
Glyphosate • Resistance to EPSP Synthase inhibitors
• Target site alteration ( e.g. , Eleusine
indica resistant to glyphosate through
mutation of Proline to serine in EPSP
synthase.)
• Differential absorption and translocation-
Lolium rigidum
• Enhanced degradation
herbicide resistance in weeds.pptx

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herbicide resistance in weeds.pptx

  • 1. PRESENTED TO Dr. N.K. CHOUBEY DEPARTMENT OF AGRONOMY PRESENTED BY SUBHASHREE MOHAPATRA M.Sc. (Agri.), 1st year DEPARTMENT OF AGRONOMY ID. No. 2231070060
  • 2. CONTENT • INTRODUCTION • RESISTANT WEED SURVEY AND CURRENT SCENARIO IN THE WORLD • DEFINITION OF HERBICIDE RESISTANCE • TYPES OF HERBICIDE RESISTANCE • FACTORS AFFECTING RESISTANCE DEVELOPMENT • MECHANISM OF HERBICIDE RESISTANCE • RESISTANCE MECHANISM TO HERBICIDE GROUPS
  • 3. INTRODUCTION Herbicide and Herbicide Resistance: • Any chemical used to kill weed or any unwanted plants in the crop field is called herbicide. • The use of chemical weed management dates back to the late 19th century when Copper Sulphate , a constituent of Bordeaux mixtures was found to kill some weeds. • Common Groundsel (Senecio vulgaris) – Atrazine was detected in Washington ( UAS ) in 1968 and was reported by Ryan in 1970.This was first report of herbicide resistance. • In India, first case was Phalaris minor developed resistance to isoproturon during 1992-93 reported by Malik and Sing. • Maximum numbers of cases of weed resistance to
  • 4.
  • 5. DEFINITION OF HERBICIDE RESISTANCE • The inherent ability of plant / biotype to survive and reproduce following exposure to a dose of herbicide normally lethal to the wild type • In a plant it may naturally occur or may get induced by such techniques as genetic engineering or selection of variants produced by tissue culture or mutagenesis.
  • 6. EXAMPLES OF HERBICIDE RESISTANCE HERBICIDE RESISTANT WEEDS Propanil Echinochloa crusgali, Echinochloa colona Chlorosulfuron Lolium rigidum , Kochia scoparia Sulfosulfuron Phalaris minor 2,4 -D Daucus carota , Commelina diffusa Simazine Lolium rigidum Isoproturon Phalaris minor, Cirsium arvense Diclofop-methyl Lolium rigidum
  • 7. RESISTANCE FACTOR • Resistance factor (GR 50) – It is based on % inhibition in dry weight of the plant. Resistance Factor = GR 50 value of resistance population GR 50 value of susceptible population Q. If the dry matter of the resistant population of Phalaris minor to Isoproturon in wheat field is estimated as 412kg where as susceptible population estimated as 238kg in 1hectare area. Determine the resistance factor and state whether isoprotruron is recommendable or not? Ans:- Dry wt. of resistant population = 412kg , Dry wt. of susceptible population = 238kg, Resistance factor = 412/238 =1.73 Thus, the value of Resistance factor is >1, so isoprotruron is absolutely recommendable to the field.
  • 8. RESISTANCE WEED SURVEY AND CURRENT SCENARIO IN THE WORLD • The Survey of herbicide resistance weeds is a major tool for management. • The purpose should be :- To monitor the occurrence of herbicide resistance weeds. To access their economic impact all over the world. • First world wide survey of herbicide resistant weeds was conducted by Homer Lebaron in 1990 & 1991.
  • 9. CHART SHOWING THE NUMBER OF WEED SPECIES WITH HERBICIDE RESISTANCE GROUPS COUNTRY WEED BIOTYPES GERMANY 19 CHINA 9 CANADA 44 UK 24 MEXICO 3 COUNTRY WEED BIOTYPES INDIA 3 FRANCE 32 USA 122 SPAIN 24 AUSTRALIA 51
  • 10. TYPES OF HERBICIDE RESISTANCE 1. Simple Resistance 2. Cross Resistance 3. Negative Cross resistance/ Collateral Sensitivity 4. Multiple Resistance 5. Reverse Resistance 6. Co- Resistance/ Compound Resistance
  • 11. SIMPLE RESISTANCE • It is simply the resistance of a weed species due to its continuous exposure to an herbicide. • In other words, it is resistance of one herbicide to one particular mechanism. Complete/full resistance • Resistance biotype are not at all affected by the herbicide used at the recommended dose. • Its growth and reproduction (seed production) continue unabated and as usual even after that herbicide application. Partial resistance ( Rubin, 1991 ) • Resistance biotypes receive severe inhibition on their vegetative growth by the herbicide used at the recommended dose. However, they continue to grow insufficiently and reach to flowering and produce some seeds.
  • 12. CROSS RESISTANCE • It evolves when a weed species already resistance to a herbicide shows resistance to other herbicides of the same chemical class to which it had never been exposed or it shows resistance to two or more herbicides due to single resistance mechanism. • Simply, resistance of two or more herbicides to single resistance mechanism. • It is of two types – Target Site- based Cross – Resistance Metabolic Cross Resistance For e.g.:- Imazethapyr resistant Setaria faberi shows cross resistance to nicosulfuron.
  • 13. Target Site – based Cross Resistance:- • Resistance to two or more herbicides of similar or dissimilar chemical groups inhibiting the same target site due to similar target site alteration. • For e.g.: found in herbicides of triazines, triazinones,phenylureas,uracils. Metabolic Cross Resistance :- • Resistance to two or more herbicides of similar or dissimilar chemical groups or their toxic metabolites due to similar rate of degradation of the herbicides. • For e.g.:- Phalaris minor shows resistance to isoproturon.
  • 14. Crop Weed With the use of Herbicide Cross Resistance Country / Region Wheat Phalaris minor Isoproturon Diclofop-p-methyl Fenoxaprop-p- ethyl Clodinafop propargyl Sulfosulfuron Punjab, Haryana Punjab, Haryana Punjab, Haryana Punjab, Haryana Wheat Alopecurus myosuroides Isoproturon Clodinafop propargyl UK
  • 15. Crop Weed With the use of Herbicide Cross Resistance Country / Region Maize, Soybean Seteria faberi Nicosulfuron Imazethapyr USA Rice Cyperus difformis Sulfonylureas Bispyribiac sodium Italy Wheat Lolium rigidum Diclofop - p - methyl Chlorosulfuron Australia
  • 16. Negative Cross-resistance/Collateral Sensitivity • It refers to the mechanism by which an individual resistant to one herbicide or a chemical family of herbicides shows higher or increased herbicides sensitivity to other herbicides than its natural wild type susceptible population. • This happens very frequently due to change in the target enzyme. The change makes enzyme more vulnerable to other herbicides inhibiting the same enzyme. • For example; the atrazine resistant biotype of Echinochloa crusgalli shows more sensitivity to fluazifop-butyl and sethoxydim.
  • 17. Multiple Resistance • It is the resistance through which a weed species shows resistance to herbicides of different chemical classes having different mode of action by two or more distinct resistance mechanisms. • Thus resistance to several herbicides resulting from two or more distinct resistance mechanisms takes place in the same plant (more than one mutation). • The classical example of multiple resistance is Lolium rigidum against various group of herbicides. • Multiple resistance was first reported in Lolium rigidum in Australia and Alopecurus myosuroides in Europe. • Alopecurus myosuroides developed resistance to chlortoluron in 1982 in U. K. and in 1983 in Germany.
  • 18. Reverse Resistance • It is a term used to describe a phenomenon or situation in which the weed biotype resistant to a herbicide fall susceptible to the very herbicide if it is not used for a Period of 7-10 years, in stead some alternative herbicides used to kill the resistant population. • It is believed to be a natural phenomenon that susceptible population becomes resistant on repeated Exposure to a herbicide and it reverts back to be susceptible one if the very herbicide is not used for sufficiently Long period.
  • 19. Co-Resistance/Compound Resistance • . Co-resistance is a term used to designate a resistance phenomenon in which a weed develops resistance to both mixing partner herbicides of a mixture applied concurrently. • This is a limitation of herbicide mixtures, which may seldom occur. • This suggests that herbicide mixture also cannot completely rule out the development of multiple resistance. • Only example so far, Lolium rigidum developed resistance to amitrole and atrazine applied to concurrently.
  • 20. FACTORS AFFECTING RESISTANCE DEVELOPMENT WEED FACTORS: 1. Initial frequency for resistance development 2. Hypersensitivity of the susceptible weed species to herbicide 3. Selection Pressure 4. Biological fitness 5. Weed Biology 6. Mode of inheritance of resistance genes
  • 21. H ER B IC ID E FA C TOR S • Application of highly potent herbicides • Specific mode of action with single target Site • Overdependence and Frequent application of herbicides without rotation • Longer residual activity in soil C R OPPIN G PR A C TIC ES • Tillage • Crop monoculture
  • 22.
  • 23. MECHANISM OF HERBICIDE RESISTANCE Exclusionary mechanism of resistance • Differential herbicide uptake • Differential translocation • Sequestration • Enhanced metabolism/degradation Target site mechanism of resistant • Altered site of action/target site alteration • Site of Over-production
  • 24. Exclusionary mechanism of resistance Exclusionary mechanism of resistance: It refers to those mechanisms which exclude or take away herbicide molecules from the site of action in plants where they induce toxic effect. Differential herbicide uptake: Herbicide resistance biotypes take up fewer amounts of herbicide molecules may be due to reduced leaf area, Waxier leaves etc. Differential translocation: Less herbicide uptake result in its less translocation, that is, Lolium rigidum resistance to chlorsulfuron. Sequestration and compartmentation: It refers to the storing, accumulation and sequestration of herbicide in vacuoles, cells or tissues away from the actual site of action of that herbicide and thus prevents the reaching of herbicide at site of action, e.g. bipyridiliums( Paraquat)
  • 25. Enhanced metabolism/ degradation: • Quick degradation of herbicide into non – toxic metabolites into the plant before reaching to the site of action. • It is found in phenylureas (isoproturon,chloroturon), ‘fop’ , ‘prop’ and ‘dim’ herbicides, bipyridiliums ( also sequestration) and triazines. (Enhanced Metabolism) (Sequestration)
  • 26. Target site mechanism of resistance Altered site of action/ target site alteration : • It is the alteration in the binding site of an herbicide due to some genetic changes in biotypes showing resistance, and this herbicide molecule do not bind to the site of action. Site of overproduction: • In this , site of action is produced in an excess amount and so normal rate of herbicide application can’t deactivate the total enzyme produced.
  • 27. Resistance Mechanism to Herbicide Groups HERBICIDE RESISTANCE MECHANISM Triazines • Resistance to PS II inhibitors. • Target site alteration/ point mutation in psbA gene. • Enhanced degradation through glutathione conjugation. (e.g., Abutilon theophrasti to atrazine) • Enhanced degradation through oxidization of Herbicide. ( e.g., Simazine resistant Lolium rigidum by cytochrome P-450 monooxygenase
  • 28. Phenylureas (isoproturon, chloroturon ) • Enhanced metabolism – e.g., Phalaris minor resistance to isoproturon through de-alkylation and ring alkyl oxidation by NADPH – cytochrome. • Target site alteration – Phalaris minor resistance to clodinafop Paraquat • Resistance to PS-I inhibitors • Detoxification of toxic products formed – (e.g., conyza bonariensis) • Rapid sequestration and compartmentation (e.g., Hordeum leporinum) Dinitroanilines • Resistance to mitotic disruptions • Target site alteration (e.g., Eleusine indica)
  • 29. Fop , prop and dim herbicides • Resistance to ACCase inhibitors. • Target site alteration (Lolium rigidum Resistance to diclofop- methyl.) • Enhanced degradation ( e.g.:- Alopecurus myosuroides) • Overproduction of ACCase . Chlorosulfuron • Resistance to ALS/AHAS inhibitors • Target site alteration (e.g., Kochias coparia) • Enhanced degradation ( Lolium rigidum)
  • 30. Glyphosate • Resistance to EPSP Synthase inhibitors • Target site alteration ( e.g. , Eleusine indica resistant to glyphosate through mutation of Proline to serine in EPSP synthase.) • Differential absorption and translocation- Lolium rigidum • Enhanced degradation