Mechanism of Wild Oat (Avena fatua L.) Resistance to Imazamethabenz-Methyl

Abstract

Abstract Imazamethabenz-methyl, an acetolactate synthase inhibitor, is used to control wild oat and blackgrass in wheat. Its selectivity is due to differential rates of metabolism to the biologically active imazamethabenz acid from the parent ester in wheat and susceptible species. Imazamethabenz-methyl is a mixture of meta - and para -isomers (2:3), with the meta -isomer being more phytotoxic to wild oat than the para -isomer. Several studies were conducted to characterize the physiological mechanism of resistance in a wild oat biotype resistant to imazamethabenz-methyl. Dose responses in greenhouse experiments indicated an ED 50 of 0.5 kg ai/ha for the susceptible wild oat biotype and 4.0 kg/ha for the resistant biotype. Acetolactate synthase enzyme extracts from the susceptible wild oat, resistant wild oat, and wheat were equally sensitive to imazamethabenz acid, with I 50 values of 2.3 × 10 −7 M, 2.5 × 10 −7 M, and 3.3 × 10 −7 M, respectively. The meta -isomer was absorbed better than the para -isomer in both resistant and susceptible biotypes, and there were only minor differences in absorption patterns of the same isomer between biotypes. Increased translocation of [ 14 C] imazamethabenz was also observed in the susceptible biotype compared to the resistant biotype. Finally, more meta -isomer was metabolized to the acid form to a greater extent in the susceptible than in the resistant biotype. Apparently, the primary mechanism of resistance to imazamethabenz-methyl in wild oat is due to reduced metabolism of imazamethabenz-methyl to the biologically active imazamethabenz acid and is not due to an altered target site.