Using Molecular Tools to Understand and Combat Herbicide Resistance.

Evolution of resistance to herbicides is a significant problem facing world agriculture. Because herbicides are so efficient and effective for weed control, many growers have over time essentially replaced all other weed control tactics with herbicides alone. This extensive reliance on a single weed control tactic has resulted in intense selection pressure for any traits enabling survival. Widespread reliance on herbicides for weed control across millions of hectares has resulted in fascinating examples of resistance evolution. Historically, most studies of evolved mechanisms of herbicide resistance uncovered simple point mutations in genes encoding herbicide target sites. These mutations generally have the effect of 1) increasing the concentration of herbicide inhibitor required to achieve sufficient enzyme inhibition (for competitive inhibitors) or 2) changing enzyme structure so that the inhibitor does not prevent access of substrates to the target site (non-competitive inhibitors). Molecular diagnostic markers have been developed for these target-site resistance (TSR) mutations, including the psbA gene (in Photosystem II), acetolactate synthase, acetyl-Co-A-carboxylase, and 5-enol-pyruvylshikimate-3-phosphate synthase (EPSPS, the target site of the herbicide glyphosate). Target-site alterations continue to be a primary way by which weeds evolve resistance, but more sophisticated target-site alterations, including a double mutation, codon deletion, and whole-gene amplification, recently have been identified and can be diagnosed using molecular markers. Non-target-site resistance (NTSR) mechanisms include those that reduce the concentration of herbicide reaching the active site, including metabolism and reduced translocation. Fewer specific genes for NTSR have been identified than for TSR, but some transcriptional and protein diagnostic markers have been developed to enable more rapid diagnosis of NTSR. These markers can be used to identify metabolic genes such as cytochrome P450s and glutathione-S-transferases that are involved in detoxifying herbicides.