Metabolism-based resistance of a wild mustard (Sinapis arvensis L.) biotype to ethametsulfuron-methyl.

Under controlled-environment conditions, ethametsulfuron-methyl doses that inhibited growth by 50% (ED(50)) were >100 and <1 g of active ingredient (ai) ha(-)(1) for ethametsulfuron-methyl-resistant (R) and -susceptible (S) wild mustard, respectively. There were no differences between the two biotypes with regard to absorption and translocation of the herbicide. Three days after treatment, approximately 90, 5, and 2% of the applied [(14)C]ethametsulfuron-methyl was found in the treated leaf, foliage, and roots of each biotype, respectively. Acetolactate synthase extracted from the two biotypes was equally sensitive to both ethametsulfuron-methyl and chlorsulfuron. These results indicate that resistance was not due to differences in the target site, absorption, or translocation. However, ethametsulfuron-methyl was metabolized more rapidly in the R than the S biotype. Approximately 82, 73, 42, 30, and 17% of the recovered radioactivity remained as ethametsulfuron-methyl in R wild mustard 3, 6, 18, 48, and 72 h after treatment, respectively. Conversely, 84, 79, 85, and 73% of the (14)C was ethametsulfuron-methyl in the S biotype 12, 24, 48, and 72 h after treatment, respectively. On the basis of these results, it is proposed that resistance is due to enhanced metabolism of ethametsulfuron-methyl in the R biotype.