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• Types of Mode of Action of herbicides


  • Acetylcholinesterase (AChE) inhibitors
  • Acetylcholine receptor (nAChR) channel blockers
  • Chloride channel antagonists/activators
  • Sodium channel modulators/blockers
  • Juvenile hormone mimics
  • Mitochondrial complex electron transport inhibitors
  • Inhibitors of mitochondrial ATP synthase
  • Inhibitors of chitin biosynthesis
  • Inhibitors of acetyl CoA
  • Nicotinic acetylcholine receptor (nAChR) antagonists or activators
  • Moulting disruptors e.g. Ecdysone receptor agonists (steroid hormone controls moulting)
• Mode of Action


  The effect of the herbicide on plant growth and eventual death at effective doses

  
• Site of Action


  Location at which a herbicide exerts its toxicity at the cellular level

  
• Mode of Action


  Relates to the Site of Action and genetically engineered plants
• Pests


  • Insects
  • Weeds
• Not treated
• Important insecticides mode of action


  • Acetylcholinesterase (AChE) inhibitors
  • Acetylcholine receptor (nAChR) channel blockers
  • Chloride channel antagonists/activators
  • Sodium channel modulators/blockers
  • Juvenile hormone mimics
  • Mitochondrial complex electron transport inhibitors
  • Inhibitors of mitochondrial ATP synthase
  • Inhibitors of chitin biosynthesis
  • Inhibitors of acetyl CoA
  • Nicotinic acetylcholine receptor (nAChR) antagonists or activators
  • Moulting disruptors e.g. Ecdysone receptor agonists (steroid hormone controls moulting)
• Important plant processes


  • Photosynthesis (food)
  • Respiration (energy)
  • Amino acids (proteins/growth)
  • Lipids (cell membranes)
  • Pigments (energy/light capture)
  • Chlorophyll, carotenoids
  • Mitosis (cell division)
• Contact and absorption


  Contact, penetration, and movement of the herbicide into the plant through the cuticle or epidermal root tissue

  
• Translocation


  Movement of the herbicide to the site of action

  
• Cellular targets of herbicide action in plants


  • Lipid Synthesis Inhibitors
  • Nitrogen Metabolism
  • Seedling Root Growth Inhibitors
  • Seedling Shoot Growth Inhibitors
  • Amino Acid Synthesis Inhibitors
  • Growth Regulators
  • Photosynthesis Inhibitors
  • Pigment Inhibitors
  • Cell Membrane Disrupters
• Herbicide Mechanisms of Action


  • Plant Growth Regulators
  • Seedling Growth Inhibitors
  • Photosynthetic Inhibitors
  • Amino Acid Synthesis Inhibitors
  • Lipid Synthesis Inhibitors
  • Cell Membrane Disruptors
  • Cell devision (Mitosis) Inhibitors
  • Pigment Inhibitors
• Auxin mimic


  Synthetic auxin that kills target weeds by mimicking the plant growth hormone auxin (indole acetic acid)
• Effective doses of auxin mimics cause uncontrolled and disorganized plant growth that leads to plant death
• Auxin-mimicking herbicides


  Affect cell wall plasticity and nucleic acid metabolism through stimulating the activity of a membrane-bound ATPase proton pump (reduce pH) and leading to disorders in RNA, DNA, and protein biosynthesis
• Acetamides


  Disrupt cell development in emerging shoot (coleoptile) during germination and emergence
• Acetamides


  Inhibit several plant processes including biosynthesis of fatty acids and lipids, and biosynthesis of proteins including gibberellins
• Triazines (Atrazine)


  Inhibit photosynthesis by binding to the QB-binding niche on the D1 protein of the photosystem II complex in chloroplast thylakoid membranes
• Atrazine binding at the PSII QB binding pocket blocks electron transport from Quinone A (QA) to Quinone B (QB) and stops CO2 fixation and production of ATP and NADPH2 which are all needed for plant growth
• Atrazine can carry over and have effects on plants
• There is resistance to Atrazine
• Paraquat


  As a herbicide, it acts by inhibiting photosynthesis by accepting electrons from photosystem I and transferring them to molecular oxygen, producing destructive reactive oxygen species
• Paraquat quickly destroys cell membranes, resulting in "leaf burn" type symptoms
• Paraquat is activated by exposure to sunlight to form oxygen compounds such as hydrogen peroxide that destroy plant tissue by rupturing cell membranes
• Perennial weeds usually regrow after paraquat treatment because there is no herbicide movement to underground root or shoot systems
• Glyphosate (Roundup)


  Inhibits the shikimic acid pathway, specifically the enzyme 5-enolpyruvoylshikimate 3-phosphate synthetase, which is necessary for the biosynthesis of the essential aromatic amino acids phenylalanine, tyrosine, and tryptophan
• Glyphosate is very nontoxic, phloem translocated, and tightly adsorbed and inactive in soil
• Genetically engineered Roundup Ready corn is resistant to glyphosate
• Long chain fatty acid inhibitors


  Inhibit acetyl-CoA carboxylase (ACCase) and disrupt early fatty acid biosynthesis, preventing the release of both unsaturated and saturated fatty acids from the plastids
• The primary site of absorption and action of long chain fatty acid inhibitors is the roots for broadleaf species and the emerging shoot for grass species
• Dicamba


  Binds to tubulin, the major microtubule protein, inhibiting polymerization of microtubules at the assembly end and causing a loss of microtubule structure and function, preventing alignment and separation of chromosomes during mitosis
• Auxin transport inhibitors (e.g. 2,4-D, naptalam)


  Inhibit polar transport of naturally occurring auxin, IAA and synthetic auxin-mimicking herbicides, causing abnormal accumulation of IAA and disrupting the delicate auxin balance needed for plant growth
• Pigment inhibitors (e.g. Bromoxynil)


  Interfere with pigment production and protection of chlorophyll, causing the affected plant parts to become white to translucent and appear bleached, and inhibit oxidative phosphorylation in mitochondria, negatively affecting plant respiration