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INDIRA GANDHI KRISHI VISHWAVIDYALAYA RAIPUR
PRESENTED BY
Ram Nath Potai
Ph D Scholar
Department of Agronomy
j
Physiological and biological aspects of herbicides
College of Agriculture, Raipur
Session- 2022-23
CLASSIFICATION OF HERBICIDES
Based on mechanism of action
HIGH RISK
(A,B)
MEDIUM RISK
(C,D,E,F)
LOW RISK
(G,H,I,K,L,M,N,O,P)
Mode of action - Lipid Inhibitors
Group -A
Fenoxaprop,
Fluazifop,
Quizalofop,
Clethodim,
Sethoxydim
 Mechanism of action -Inhibits ACCase, (Acetyl- CoA
carboxylase) block fatty acid synthesis needed for membranes,
stops growth
Symptoms-
Growing point rots, new leaves pull out easily
Chlorosis to necrosis, Growing point separates
Imazamox, Imazapic
Imazethapyr, Imazaquin
Cloransulam, flumetsulam
Mechanism of action-
Inhibit Acetolactate synthase (ALS), blocks amino
acid synthesis needed for proteins synthesis
A herbicide which inhibits the production of amino acids
Symptoms-
• Inhibited growth.
• Foliar chlorosis and necrosis within 4-24 days.
Mode of action- Amino Acid Inhibitors
Group -B
Atrazine, Simazine, Metribuzin
Linuron, Bromoxynil, Bentazon
Mechanism of action-
Herbicides inhibit photosynthesis-II by binding to
D1 proteins of the photosystem II complex in chloroplast
thylakoid membranes. Herbicide binding at this protein blocks
electron transport and stops CO2 fixation and production of
energy needed for plant growth the death of plants, Block
photosynthesis, stops production of sugars,
Unused light energy destroys cell membranes
Symptoms- Chlorosiss/necrosis of leaf tips
Contact burn of treated leaves
Mode of action-Photosynthesis inhibitors
Group - C
Mode of action- Cell Membrane Disrupters
Goup- D
Paraquat
Diquat
Mechanism of action- Photosystem – I Protoporphyrinogen
oxidase (PPO) creates membrane destroying compounds,
destroys cells
Symptoms-
These herbicide destroy cell membranes which leads to the
breakdown of cells.
Oxidation of cell membranes by free radicals of oxygen.
Chlorotic veins, contact burn of treated leaves
Mode of action -Pigment Inhibitors
Group –F
Tembotrione, Mesotrione,
Topramezone, Clomazone,
Isoxaflutole,
Pigment inhibitors prevent plant from forming photosynthetic
pigments. As a result the affected plant parts become white to
translucent
Mechanism of action- Phytoene and phytofluene desaturas
enzymes of the terpenoid pathway.
 Inhibits carotene synthesis, leads to chlorophyll destruction and
bleached (white) plants
Mode of Action: Amino Acid Synthesis Inhibitors
Group -G
Glyphosate
Sulfonate
Anilofos
Mechanism of action- Inhibits (5- enol pyruvoyl shikimate -3-
phosphate (EPSP) blocks amino acid synthesis needed for
protein synthesis
• Translocated to growing points, new growth injure first
• Chlorosis to necrosis (Yellowing to death)
Mode of action- Folic acid synthesis Inhibition
Group -I
Asulam (Carbamates)
Mechanism of action- Dihydropteroate (DHP) Synthase
Inhibition
Mode of action – Cell division
Group K-1
Pendimethalin,
Trifluralin
Ethalfluralin
Mechanism of action-
Microtubule assembly inhibition (seedling root inhibition)
Tubulin protein involved in cell division block cell division, no
growth of seedlings
Injury root tips and hypocotyl
Gererally annual grasses controlled plus some broadleaves
Cell Division Inhibitors
Group K-2
Acetochlor, Alachlor
Dimethanamid, Metolachlor
Pyroxasulfone
Mechanism of action-
Cell Division Inhibitors (Seedling Shoot growth inhibit)
Stunting of shoots that result in abnormal seedling that do not
emerge from the soil.
leafing out, buggy whipping
Mode of Action: Oxidative Phosphorylation Uncouplers
Group- M
Dinoseb
Dinoterb
Mechanism of action- Uncoupling (Membrane disruptors)
Mode of action- Plant growth regulators (PGR)
Group- O
Dicamba
2,4-D
MCPA
2,4-DB
Clopyralid
Mechanism of action -Synthetic auxins mimicking the action
of indole acetic acid
 Epinasty downward twisting, abnormal leaf and stem growth,
death
CONCLUSION
 Understand the physiology of herbicides would be of great
help to tackle the problem of resistance.
 Preventing and managing herbicide resistance
 Planning weed management programs- match the herbicide to
the weed problem
 Understanding of how herbicides perform in weeds
 Improving herbicides performance
Thank you

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physiolgical & biological aspects of herbicidess.pptx

  • 1. INDIRA GANDHI KRISHI VISHWAVIDYALAYA RAIPUR PRESENTED BY Ram Nath Potai Ph D Scholar Department of Agronomy j Physiological and biological aspects of herbicides College of Agriculture, Raipur Session- 2022-23
  • 2. CLASSIFICATION OF HERBICIDES Based on mechanism of action HIGH RISK (A,B) MEDIUM RISK (C,D,E,F) LOW RISK (G,H,I,K,L,M,N,O,P)
  • 3. Mode of action - Lipid Inhibitors Group -A Fenoxaprop, Fluazifop, Quizalofop, Clethodim, Sethoxydim  Mechanism of action -Inhibits ACCase, (Acetyl- CoA carboxylase) block fatty acid synthesis needed for membranes, stops growth Symptoms- Growing point rots, new leaves pull out easily Chlorosis to necrosis, Growing point separates
  • 4. Imazamox, Imazapic Imazethapyr, Imazaquin Cloransulam, flumetsulam Mechanism of action- Inhibit Acetolactate synthase (ALS), blocks amino acid synthesis needed for proteins synthesis A herbicide which inhibits the production of amino acids Symptoms- • Inhibited growth. • Foliar chlorosis and necrosis within 4-24 days. Mode of action- Amino Acid Inhibitors Group -B
  • 5. Atrazine, Simazine, Metribuzin Linuron, Bromoxynil, Bentazon Mechanism of action- Herbicides inhibit photosynthesis-II by binding to D1 proteins of the photosystem II complex in chloroplast thylakoid membranes. Herbicide binding at this protein blocks electron transport and stops CO2 fixation and production of energy needed for plant growth the death of plants, Block photosynthesis, stops production of sugars, Unused light energy destroys cell membranes Symptoms- Chlorosiss/necrosis of leaf tips Contact burn of treated leaves Mode of action-Photosynthesis inhibitors Group - C
  • 6. Mode of action- Cell Membrane Disrupters Goup- D Paraquat Diquat Mechanism of action- Photosystem – I Protoporphyrinogen oxidase (PPO) creates membrane destroying compounds, destroys cells Symptoms- These herbicide destroy cell membranes which leads to the breakdown of cells. Oxidation of cell membranes by free radicals of oxygen. Chlorotic veins, contact burn of treated leaves
  • 7. Mode of action -Pigment Inhibitors Group –F Tembotrione, Mesotrione, Topramezone, Clomazone, Isoxaflutole, Pigment inhibitors prevent plant from forming photosynthetic pigments. As a result the affected plant parts become white to translucent Mechanism of action- Phytoene and phytofluene desaturas enzymes of the terpenoid pathway.  Inhibits carotene synthesis, leads to chlorophyll destruction and bleached (white) plants
  • 8. Mode of Action: Amino Acid Synthesis Inhibitors Group -G Glyphosate Sulfonate Anilofos Mechanism of action- Inhibits (5- enol pyruvoyl shikimate -3- phosphate (EPSP) blocks amino acid synthesis needed for protein synthesis • Translocated to growing points, new growth injure first • Chlorosis to necrosis (Yellowing to death)
  • 9. Mode of action- Folic acid synthesis Inhibition Group -I Asulam (Carbamates) Mechanism of action- Dihydropteroate (DHP) Synthase Inhibition
  • 10. Mode of action – Cell division Group K-1 Pendimethalin, Trifluralin Ethalfluralin Mechanism of action- Microtubule assembly inhibition (seedling root inhibition) Tubulin protein involved in cell division block cell division, no growth of seedlings Injury root tips and hypocotyl Gererally annual grasses controlled plus some broadleaves
  • 11. Cell Division Inhibitors Group K-2 Acetochlor, Alachlor Dimethanamid, Metolachlor Pyroxasulfone Mechanism of action- Cell Division Inhibitors (Seedling Shoot growth inhibit) Stunting of shoots that result in abnormal seedling that do not emerge from the soil. leafing out, buggy whipping
  • 12. Mode of Action: Oxidative Phosphorylation Uncouplers Group- M Dinoseb Dinoterb Mechanism of action- Uncoupling (Membrane disruptors)
  • 13. Mode of action- Plant growth regulators (PGR) Group- O Dicamba 2,4-D MCPA 2,4-DB Clopyralid Mechanism of action -Synthetic auxins mimicking the action of indole acetic acid  Epinasty downward twisting, abnormal leaf and stem growth, death
  • 14. CONCLUSION  Understand the physiology of herbicides would be of great help to tackle the problem of resistance.  Preventing and managing herbicide resistance  Planning weed management programs- match the herbicide to the weed problem  Understanding of how herbicides perform in weeds  Improving herbicides performance