Mechanism of wild oat (Avena fatua L.) resistance to imazamethabenz-methyl

Imazamethabenz-methyl, an acetolactate synthase inhibitor, is used to contr ol wild oat and blackgrass in wheat. Its selectivity is due to differential rates of metabolism to the biologically active imazamethabenz acid from th e 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 p hytotoxic to wild oat than the para-isomer. Several studies were conducted to characterize the physiological mechanism of resistance in a wild oat bio type resistant to imazamethabenz-methyl. Dose responses in greenhouse exper iments indicated an ED50 of 0.5 kp ai/ha for the susceptible wild oat bioty pe and 4.0 kg/ha for the resistant biotype. Acetolactate synthase enzyme ex tracts from the susceptible wild oat, resistant wild oat, and wheat were eq ually sensitive to imazamethabenz acid, with I-50 values of 2.3 x 10(-7) M, 2.5 x 10(-7) M, and 3.3 x 10(-7) M, respectively. The meta-isomer was abso rbed 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 [C-14] imazamethabenz w as also observed in the susceptible biotype compared to the resistant bioty pe. Finally, more meta-isomer was metabolized to the acid form to a greater extent in the susceptible than in the resistant biotype. Apparently, the p rimary mechanism of resistance to imazamethabenz-methyl in wild oat is due to reduced metabolism of imazamethabenz-methyl to the biologically active i mazamethabenz acid and is not due to an altered target site. (C) 2000 Acade mic Press.