Search

The mechanisms of herbicide resistance were investigated in two diclofop-methyl-resistant Lolium spp. populations from central Italy, Roma ’94 and Tuscania ’97. These two populations were compared with two susceptible Italian populations (Vetralla ’94, Tarquinia ’97) and a resistant and a susceptible population from Australia, SLR31 and VLR1. The activity of acetyl Co-A carboxylase (ACCase) extracted from susceptible (S) or resistant (R) individuals from the Italian populations was inhibited by both aryloxyphenoxypropanoate (diclofop acid and fluazifop acid) and cyclohexanedione (sethoxydim) herbicides. Diclofop-methyl was rapidly de-esterified to diclofop acid at a similar rate in both R and S populations. In all populations, diclofop acid was subsequently degraded to other metabolites. The rate of degradation of diclofop acid was not significantly faster in R than in S populations; however, diclofop acid was degraded more completely in Roma ’94 and Tuscania ’97 compared with the S populations. Application of the mixed-function oxidase inhibitor 1-aminobenzotriazole (ABT) significantly enhanced diclofop-methyl toxicity towards both R populations, but not in S populations. However, enhanced herbicide metabolism does not completely account for the measured resistance level. A mechanism other than an altered ACCase and enhanced herbicide metabolism appears to be responsible for resistance to diclofop-methyl in Roma ’94 and Tuscania ’97. [ABSTRACT FROM AUTHOR]