📈 Herbicide Selectivity and Mode of Action
Herbicide Selectivity and Mode of Action — ALS inhibitors, ACCase inhibitors, PSII inhibitors, EPSPS inhibitors, and auxin mimics.
This lesson builds core elective concepts in BSc Agriculture with practical applications and exam-oriented clarity.
Herbicide Selectivity and Mode of Action
The mode of action (MoA) describes how a herbicide disrupts a specific physiological process in the target weed. Understanding MoA is essential for selecting herbicides, managing resistance, and rotating chemical groups.
ALS/AHAS Inhibitors (Group 2)
Acetolactate synthase inhibitors block the enzyme responsible for synthesis of branched-chain amino acids (valine, leucine, isoleucine):
- Chemical families: sulfonylureas, imidazolinones, triazolopyrimidines
- Examples: metsulfuron-methyl, chlorimuron-ethyl, imazethapyr
- Effective at very low doses (2-10 g/ha for sulfonylureas)
- Selectivity: crops metabolise these herbicides via cytochrome P450 enzymes
- Most resistance-prone group globally
ACCase Inhibitors (Group 1)
Acetyl-CoA carboxylase inhibitors block fatty acid synthesis in grasses:
- Chemical families: aryloxyphenoxypropionates (FOPs), cyclohexanediones (DIMs)
- Examples: fenoxaprop, clodinafop, sethoxydim
- Grass-specific — safe on all broadleaf crops (soybean, cotton, pulses)
- Used to control Phalaris minor and Avena fatua in wheat
Photosystem II (PSII) Inhibitors (Group 5/6/7)
These herbicides block electron transport in Photosystem II of chloroplasts:
| Chemical Family | Examples | Crops |
|---|---|---|
| Triazines | Atrazine, simazine | Maize, sugarcane |
| Ureas | Isoproturon, diuron | Wheat, cotton |
| Nitriles | Bromoxynil | Wheat, barley |
- Symptoms: chlorosis followed by necrosis starting at leaf margins
- Selectivity based on root uptake depth and metabolic detoxification in crops
EPSPS Inhibitors (Group 9)
5-enolpyruvylshikimate-3-phosphate synthase inhibitors block the shikimate pathway, preventing synthesis of aromatic amino acids:
- Glyphosate is the sole commercial EPSPS inhibitor
- Non-selective, systemic — kills virtually all plant species
- Widely used for pre-plant burndown, zero-tillage systems, orchard weed control
- Glyphosate-resistant (Roundup Ready) crops were developed via transgenic introduction of a resistant EPSPS gene
Synthetic Auxins (Group 4)
Auxin mimics cause uncontrolled cell elongation in broadleaf weeds:
- Examples: 2,4-D, dicamba, picloram, fluroxypyr
- Symptoms: stem twisting (epinasty), leaf curling, swollen nodes
- Selective in grasses — monocots rapidly deactivate synthetic auxins
- 2,4-D is among the oldest and most widely used herbicides in India
Other Important Groups
- PPO inhibitors (Group 14) — oxyfluorfen, fomesafen; cause rapid membrane disruption
- Microtubule inhibitors (Group 3) — pendimethalin, trifluralin; prevent cell division in root tips
- Glutamine synthetase inhibitors (Group 10) — glufosinate; causes ammonia accumulation
Rotating herbicides across different MoA groups is the cornerstone of resistance management.
Summary Cheat Sheet
| Topic | Key takeaway |
|---|---|
| Main focus | Herbicide Selectivity and Mode of Action — ALS inhibitors, ACCase inhibitors, PSII inhibitors, EPSPS inhibitors, and auxin mimics. |
| Section context | Revise this lesson with the rest of Weed Management for stronger conceptual continuity. |
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