Chapter 5 – Physiology of Weed Control by Herbicides

Structural and Biochemical Changes Due to Herbicides

• Herbicides possess a wide range of chemical structures, allowing diverse modes of action (MOA).

• Core principle: they disrupt one or more essential plant processes, leading to injury, growth suppression, or death.

• Target levels of interference

  • Structural: e.g., cell walls, membranes, microtubules.

  • Biochemical: e.g., enzymes in amino-acid, pigment, lipid synthesis.

• End-results include inhibition of cell division, membrane leakage, oxidative damage and starvation.

Baseline Biochemical Processes in Plant Cells (targets for herbicides)

• Amino-acid synthesis → proteins (build new cells, enzymes).

• Pigment synthesis → chlorophyll, carotenoids (capture light for photosynthesis).

• Lipid metabolism → forms cellular & organelle membranes, cuticular wax, energy storage.

• Transport systems

  • $xylem$ for water.

  • $phloem$ for assimilates & phytohormones.

Herbicide Sites of Action by Organelle / Cellular Structure

• Vacuole / nucleus / microtubule–spindle apparatus

  • Non-translocated soil herbicides: microtubule inhibitors (dinitroanilines).

• Mitochondria

  • Fatty acid/lipid synthesis blockers (acetamides, thiocarbamates).

  • Symplastic foliar ACCase inhibitors: aryloxyphenoxypropionate (FOPs) & cyclohexanedione (DIMs).

• Chloroplasts

  • Non-translocated foliar PPO (Protox) inhibitors.

  • Non-translocated foliar PSI electron diverters (bipyridiliums).

  • Symplastic foliar carotenoid inhibitors.

  • Apoplastic soil PSII inhibitors (triazines, ureas).

• Ribosomes

  • Non-translocated foliar glutamine synthetase inhibitor (glufosinate).

  • Symplastic foliar amino-acid/protein synthesis inhibitors (glyphosate, ALS inhibitors).

• Cell wall / plasma membrane

  • Desiccation/lipid degradation herbicides.

  • Cellulose biosynthesis blockers (diclobenil, isoxaben, quinclorac).

• Miscellaneous cytosolic interference

  • Synthetic auxins (2,4-D) & auxin transport blockers.

  • Folic-acid/vitamin synthesis blockers (asulam).

Non-Translocated (Contact) Herbicides

Foliar Applied PPO (Protox) Inhibitors

• Mode: block conversion of protoporphyrinogen IX → protoporphyrin IX (chlorophyll precursor).

• In light, excess singlet oxygen forms → lipid & protein oxidation → membrane rupture.

• Rapid symptomology: chlorosis → desiccation & necrosis within 1–3 days.

• Chemical families & examples

  • Diphenyl ether: acifluorfen.

  • Oxadiazole: oxadiazon.

  • N-phenyl-phthalimide: flumiclorac.

  • Thiadiazole: fluthiacet.

  • Triazolinone: sulfentrazone.

• Glutamine synthetase inhibitors (glufosinate) often grouped with contact herbicides—ammonia accumulation is phytotoxic.

Soil Applied, Non-translocated Herbicides

• Microtubule inhibitors: dinitroanilines (trifluralin).
  • Prevent spindle formation → block mitosis, especially in root/shoot meristems.

• Fatty-acid synthesis/cell division inhibitors

  • Chloroacetamides (alachlor, metolachlor), oxyacetamide (flufenacet), thiocarbamates (eptam).

  • Manifested by reduced cuticular wax, shorter coleoptiles, failed germination.

• Cellulose synthesis inhibitors

  • Diclobenil, isoxaben, quinclorac.

• Key agronomic note: Trifluralin must be soil-incorporated (photosensitive & volatile).

Symplastically Translocated (Systemic) Herbicides

Synthetic Auxins (Phenoxy, Benzoic, Pyridine, Quinoline acids)

• Mimic excess $IAA$, deregulate growth genes, stimulate ethylene & ABA.

• Visible effect within hours: epinasty (twisting/downward curvature), leaf strapping, stem swelling.

• Plants literally “grow themselves to death.”

• Examples: 2,4-D, MCPA, dicamba, picloram, quinclorac.

Auxin Transport Inhibitors

• Block polar auxin movement → endogenous auxin accumulation.

• Symptoms resemble synthetic auxins.

• Naptalam, diflufenzopyr.

Amino-acid Biosynthesis Inhibitors

1. Aromatic amino acids (EPSPS inhibitor)

   • Glyphosate blocks EPSP synthase → no $\text{tyrosine, tryptophan, phenylalanine}$ > halted cell-wall lignin & protein synthesis.

   • Symptoms: slow yellowing from newest leaves outward → systemic necrosis.

2. Branched-chain amino acids (ALS/AHAS inhibitors)

   • Block $\text{valine, leucine, isoleucine}$.

   • Highly potent at <10\,\text{g ai ha}^{-1}.

   • Families: sulfonylureas (chlorsulfuron), imidazolinones (imazapyr), triazolopyrimidines (flumetsulam), etc.

3. Fatty-acid synthesis in grasses (ACCase inhibitors)

   • FOPs (fluazifop) & DIMs (sethoxydim).

   • Meristem tissue browning at node region.

Miscellaneous Systemic Herbicides

• Organic arsenicals (MSMA, DSMA): contact-like burn; extremely toxic to mammals.

• Folic-acid pathway inhibitors: asulam blocks $7,8$-dihydropteroate synthase.

Herbicidal Effects on Photosystems (Learning Objective 5.2)

Photosystem I Electron Diverters (Contact, Foliar)

• Bipyridiliums (paraquat, diquat) accept electrons from PSI → form radical + $H<em>2O</em>2$.

• Rapid membrane peroxidation → tissue dries within hours (“flash burn”).

Carotenoid Biosynthesis (Bleachers)

• Carotenoids normally quench singlet oxygen & protect chlorophyll.

• Inhibitors (e.g., norflurazon) → new leaves emerge white then die.

• Systemic (symplastic) movement allows whole-plant bleaching.

Photosystem II Inhibitors

1. Classical (apoplastic)

   • Bind $Q<em>B$ site on $D</em>1$ protein, stop electron flow & $CO_2$ fixation.

   • Families: triazines (atrazine), ureas (diuron), uracils (terbacil), amides (propanil), etc.

   • Down-stream: reactive oxygen species → membrane leakage → chlorosis → necrosis.

2. Rapid-acting PSII inhibitor (benzothiadiazole: bentazon) – similar endpoint but faster.

Herbicide Groups & Representative MOA (from slide table)

• See bullets above; classification highlights importance for resistance-management rotations.

• Example cross-link: aryloxyphenoxy-alkanoic esters (FOPs) fall in ACCase inhibition group.

Key Biological Keywords / Processes

• “Food” for plant = photosynthesis efficiency.

• Pigments = energy capture; herbicide can darken or bleach.

• Amino acids → proteins → metabolism.

• Cell wall rigidity (cellulose) & membrane integrity (lipids).

• Hormone balance (auxin) steers growth/development.

Herbicide Symptomology (Learning Objective 5.3)

• Non-translocated contact: initial burn at spray point, requires thorough coverage, surviving tissue resumes normal growth.

• Apoplastic (PSII): older leaves first, general chlorosis then necrosis.

• Symplastic (bleachers, amino-acid inhibitors, auxins): symptoms begin in new growth because herbicide moves with assimilates.

• Inorganic (copper, arsenic): plasmolysis/scorching.

Herbicide Toxicity Classes & Types

• WHO classification on labels

  • Class Ia: “very highly poisonous,” skull & crossbones.

  • Class Ib: “highly poisonous,” skull & crossbones.

  • Class II: “poisonous.”

  • Class III: “harmful.”

  • Class IV: unlabelled / low hazard.

• Acute toxicity: rapid damage (minutes–hours) common in contact herbicides (paraquat, bromoxynil, diquat).

• Chronic toxicity: delayed, associated with systemic herbicides.

Herbicide Resistance (Learning Objective 5.4)

• Definition: formerly susceptible population survives herbicide doses previously lethal.

• Cellular mechanisms

  • Metabolic detoxification (inactivation).

  • Adsorption to cell wall (reduced availability).

  • Conjugation to glucose/amino acid.

  • Non-enzymatic chemical degradation (hydrolysis, carboxylation).

• MOA predisposed to resistance (documented cases)

  • ALS inhibitors.

  • ACCase inhibitors.

  • PSII inhibitors (triazines).

  • Microtubule inhibitors (dinitroanilines).

Herbicide-Resistant Crops (HRC)

• Mutation/selection breeding: Clearfield rice (imidazolinone resistant; collab MARDI–LSU AgCenter).

• Transgenic (genetic engineering)

  • Roundup Ready® soybean (glyphosate-tolerant).

  • LibertyLink® corn (glufosinate-tolerant).

  • Mechanism: insert gene that bypasses herbicide-blocked metabolic step.

Benefits of HRC

1. Reduced crop loss from herbicide injury → higher yield.

2. Simplified control of difficult weeds.

3. Enabling use of relatively eco-benign herbicides (e.g., glyphosate).

4. Lower production costs (fewer passes, less tillage).

Concerns & Ethical / Environmental Implications

• Evolution/selection of herbicide-resistant weeds (“super weeds”).

• Gene flow to wild relatives → ecological imbalance.

• Adventitious presence in non-GM crops—market/trade impacts.

• Human health & non-target organism impacts of GMO.

• HRC volunteers can themselves become weeds.

• Public perception & loss of trust in food system.

Resistance Management Best-Practices

1. Crop rotation.

2. Integrate non-chemical controls (tillage, cover crops).

3. Mix herbicides with different MOA.

4. Sequential applications through season.

5. Rapid containment of resistance foci.

Practical Connections / Real-World Relevance

• Herbicide labels now list “Group number” corresponding to MOA to aid rotation planning.

• Understanding MOA allows diagnosis of field injury symptoms (important for extension agents, crop scouts).

• Environmental stewardship: choosing contact vs systemic herbicides influences risk of off-target drift & groundwater residue.

• Regulatory toxicology (acute vs chronic) guides PPE requirements.

• Ethical debate around GM crops mirrors broader societal concerns on sustainability and corporate control of seed technology.

Quick Reference Formulas & Numerical Data

• EPSPS reaction blocked by glyphosate:
  $\text{shikimate-3-phosphate} + \text{phosphoenolpyruvate} \xrightarrow{EPSPS} 5\text{-enolpyruvylshikimate-3-phosphate} + \text{Pi}$

• ALS reaction (simplified):
  $2\,\text{pyruvate} \xrightarrow{ALS} 2\text{-acetolactate} + \text{CO}_2$

• Potency note: many ALS inhibitors are active at <10 \, \text{g ai ha}^{-1}.

(End of comprehensive study notes for Chapter 5 – Physiology of Weed Control by Herbicides)