ABSTRACT
Herbicides are phytotoxins used by humans to kill unwanted vegetation. Understanding the molecular sites of action of herbicides can be crucial in the production of an herbicide-resistant crop (HRC). This chapter deals with the physiological and biochemical mechanisms of natural and evolved resistance to herbicides. Both crops and weeds are naturally resistant to many selective herbicides. The mechanisms of preexisting, natural resistance of weeds and crops to herbicides are often the same for a particular herbicide. Herbicide resistance can be due to three basic mechanisms: resistance at the site of action, metabolic detoxification, and prevention of herbicide from reaching the site of action. Plants synthesize all of their essential amino acids. There are commercial herbicides that target three enzymes involved in amino acid synthesis: glutamine synthetase (GS), acetolactate synthase (ALS), and enolpyruvylshikimatephosphate synthase (EPSP synthase). Several different classes of herbicides have been reported to interfere with some aspect of lipid biosynthesis. These include the aryloxyphenoxypropionates, cyclohexanediones, pyridazinones, thiocarbamates, and chloroacetamides.
