Learning Outcomes
Students are expected to know:
• the molecular basis of herbicide mode of action and the molecular basis of herbicide selectivity within plants.
• the factors reducing the selectivity of herbicides and symptoms of toxicity in crops.
• the molecular basis of herbicide interactions with other herbicides or pesticides or synergistic or antagonistic or surfactant or antiphytotoxic substances.
• the effects of herbicides on agriculture, humans and the environment.
• the physicochemical properties and mode of action of herbicides
• the genetic, biochemical and physiological basis of weed resistance mechanisms to herbicides.
• resistant weeds in the country and worldwide.
• weed resistance management. the genetic and biochemical basis of plant resistance mechanisms (modified by classical breeding or genetic engineering) to herbicides and their effects on agriculture, humans and the environment.
Course Content (Syllabus)
Molecular (biochemical, physiological, genetic) basis of herbicides mode of action (absorption, translocation, accumulation at the site of action, binding to the protein target of action, process inhibition, deregulation of cell function, toxicity symptoms in plants). Molecular (biochemical, physiological, genetic) basis of herbicide selectivity (metabolism, reduced absorption-translocation-accumulation at the site of action, inability to bind to the protein target of action due to modification) within plants. Herbicide selectivity-reducing factors and crop toxicity symptoms. Molecular (biochemical, physiological, genetic) basis of herbicide interactions with other herbicides or plant protection products, or substances with synergistic, antagonistic, surfactant, or antiphytotoxic activity. Herbicides’ effects on agriculture, humans and the environment. Physicochemical properties and mode of action of herbicides that inhibit photosystem II (PS II)]. Physicochemical properties and mode of action of herbicides that inhibit the function of photosystem I (PS I), the biosynthesis of chlorophyll (enzyme PPG-O) or carotenoids (enzyme PDS, 4-HPPD, DOXP). Physicochemical properties and mode of action of herbicides that inhibit the biosynthesis of fatty acids (ACCase enzyme or fatty acid elongases enzymes). Physicochemical properties and mode of action of herbicides that inhibit branched chain amino acid biosynthesis of carbon atoms (ALS or AHAS enzyme). Physicochemical properties and mode of action of herbicides that inhibit aromatic amino acid biosynthesis (EPSPS enzyme) or glutamine biosynthesis (GS enzyme). Physicochemical properties and mode of action of herbicides that inhibit mitosis (tubulin protein) or cell division (elongase enzymes). Physicochemical properties and mode of action of herbicides that inhibit cellulose biosynthesis (CESA enzyme) or herbicides with synthetic-auxin action (TIR1, protein receptor of auxin). Genetic, biochemical and physiological basis of herbicide resistance mechanisms. Herbicide resistant weeds in the country and worldwide. Herbicide resistance management. Genetic and biochemical basis of herbicide tolerance mechanisms in plants (modified by classical breeding or genetic engineering) and their effects on agriculture, humans and the environment. Summary-conclusions on herbicide modes of action and selectivity. Work presentations by postgraduate students.