Multiple mechanisms and multiple herbicide resistance in Lolium rigidum

Herbicide resistance in the grass weed Lolium rigidum is widespread across the cropping regions of southern Australia creating a serious practical problem for the control of this species. One biotype shows resistance to herbicides from nine chemical classes with five modes of action. This biotype contains two herbicide-resistant target sites, acetolactate synthase (ALS) and acetyl-coenzyme A carboxylase (ACCase); however, resistant ALS is restricted to about 5 % of the population. In addition, this population has enhanced capacity for detoxification of the herbicides chlorotoluron, simazine, chlorsulfuron, tralkoxydim and diclofop-methyl. This enhanced herbicide metabolism can be decreased by pre-treatment of plants with inhibitors of cytochrome P450 monooxygenases. There are differences in the synergistic effectiveness of these inhibitors between herbicides. For example, piperonyl butoxide inhibits metabolism of chlorotoluron and simazine, but not the other herbicides. These patterns indicate that while a single isozyme may be responsible for enhanced metabolism of chlorotoluron and simazine, different isozymes are responsible for enhanced metabolism of chlorsulfuron, diclofop-methyl, and tralkoxydim. Therefore, multiple resistance in this biotype is due to the accumulation of multiple mechanisms of resistance, probably encoded by several genes.