Molecular mechanisms of herbicide resistance

Mechanisms of herbicide resistance include modified target site, enhanced detoxification, and alterations in the uptake, translocation, or compartmentalization of the chemical. Triazine resistance, one of the most prevalent types of herbicide resistance found in weeds, is due to a modification at the target site, the D1 protein of photosystem II: in chloroplasts. The phenylurea herbicide chlortoluron is metabolized in wheat and barley via ring-methyl hydroxylation and N-demethylation. Resistance of these crops to the herbicide has been attributed largely to ring-methyl hydroxylation probably catalized by cytochrome P450. When P4501A1/yeast reductase fused enzyme was placed in tobacco plants, the transgenic plants showed resistance to chlortoluron and metabolized it more rapidly than did control plants, mainly via ring-methyl hydroxylation as well as N-demethylation. When mt P4501A1 and its fused enzyme with yeast reductase were each expressed in potato plants, both transgenic plants showed resistance to the herbicides chlortoluron and DCMU. Since mammals contain a large number of P450 species with overlapping broad substrate-specificity towards xenobiotics, expression of each of these species in plants seems to produce transgenic plants not only resistant to herbicides but also enhanced in metabolism of various environmental contaminants.