Herbicidal resistance formation

Most of the enzymes that catalyze the formation of xenobiotic conjugates in plants have not been well-studied. Since some conjugation reactions are involved in herbicide selectivity, it is likely that research relating to these enzymes will intensify as a result of efforts to develop herbicide resistant crops through bioengineering. Enzymes that may be useful in bioengineering for herbicide resistance are the GST enzymes, N-glucosyl transferases. 

Interfering with protein function using specific inhibitors or antibodies. There are many protein inhibitors of metabolic enzymes that, when overexpressed, could have the potential to inhibit specific enzymatic steps (e.g., Ref. ). Nonprotein inhibitors of metabolic enzymes are also extensively used, resulting in some potent plant herbicides for which resistance can be easily manipulated, or in the formation of new compounds, when nonessential pathways are inhibited. ]... 

Metflurazon inhibits photosynthesis and prevents the development of chloro-plastids in sensitive plants (Hilton et al., 1969). The authors also report on their investigation of the mode of action of 4 pyridazinone herbicides on barley. Metflurazon and its phenyl- and unsubstituted amino analogues, structurally similar to pyrazon, also inhibited the Hill reaction and photosynthesis, but showed two further biological features they resisted metabolic oxidation and inhibited chloroplast formation. The latter effect is similar to that of amitrol and dichlormate, but 100-1000 times stronger. 

Phytotoxic diloroacetamides provided a linear relationship between severe inhibition of growth and inhibition of the incorporation of [ CJoleic acid into VLCFAs in Scenedesmus acutus [7]. In higher plants, the incorporation of [ C] stearic acid or malonyl-CoA into VLCFAs was inhibited by diloroacetamides while the formation of fatty acids up to Cig was not influenced [8]. Acyl elongation with 20 0-CoA and 18 0-CoA primer substrates was inhibited by the active (S)-enantiomer of metolachlor but not by the (R)-isomer [1, 9). Inhibition of VLCFA formation was also observed in metazachlor-resistance mutant (Mz-1) cells of S. acutus [9]. Thus, the phytotoxic action of chloroacetamide herbicides is most likely by the inhibition of VLCFA synthesis. 

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