An Avena sterilis biotype was found to be highly resistant to aryloxyphenoxypropionate (APP) herbicides, especially diclofop-methyl. At the enzyme level, this biotype contained a modified acetyl-coenzyme A carboxylase (ACCase) with six-fold resistance to diclofop acid. Absorption and translocation of [C-14]diclofop-methyl applied to the leaf axil of the two-leaf stage plants were similar in both susceptible and resistant biotypes. However, the rate of metabolism of [C-14]diclofop was increased 1.5-fold in this resistant biotype compared to the susceptible. Experiments with tetcyclacis, a cytochrome P450 monooxygenase inhibitor, indicated that inhibition of this enhanced diclofop metabolism increased diclofop-methyl phytotoxicity in this biotype. Studies with ten individual families of the resistant biotype indicated that both mechanisms of resistance, an altered target site and enhanced metabolism, are present in each individual of the population. Hence, it is likely that these two mechanisms of resistance both contribute to resistance in this biotype.
|Publication status||Published - 1997|