A biotype of Avena sterilis ssp. ludoviciana is highly resistant to a range of herbicides which inhibit a key enzyme in fatty acid synthesis, acetyl-CoA carboxylase (ACCase). Possible mechanisms of herbicide resistance were investigated in this biotype. Acetyl-CoA carboxylase from the resistant biotype is less sensitive to inhibition by herbicides to which resistance is expressed. I,, values for herbicide inhibition of ACCase were 52 to 6 times greater in the resistant biotype than in the susceptible biotype. This was the only major difference found between the resistant and susceptible biotypes. The amount of ACCase in the meristems of the resistant and susceptible is similar during ontogeny and no difference was found in distribution of ACCase between the two biotypes. Uptake, translocation and metabolism of [C-14]diclofop-methyl were not different between the two biotypes. In vivo, ACCase activity in the meristems of the susceptible biotype was greatly inhibited by herbicide application whereas only 25% inhibition occurred in the resistant biotype. Depolarisation of plasma membrane potential by 50 mu M diclofop acid was observed in both biotypes and neither biotype showed recovery of the membrane potential following removal of the herbicide. Hence, a modified form of ACCase appears to be the major determinant of resistance in this resistant wild oat biotype.
|Journal||Plant and Cell Physiology|
|Publication status||Published - 1994|