Imazamethabenz-resistant wild oat ( Avena fatua L.) is resistant to diclofop-methyl

Abstract

An imazamethabenz-resistant wild oat accession AR1 was found to be resistant to diclofop-methyl. Experiments were conducted to determine the response of this accession to other acetyl-CoA-carboxylase-inhibiting herbicides and the physiological mechanism of its resistance to diclofop-methyl. Diclofop-methyl dose responses in greenhouse experiments indicated an ED 50 of 1.04 kg ha −1 for the AHS2 susceptible accession and 43.8 kg ha −1 for the AR1 resistant accession with a AR1/AHS2 ED 50 ratio of 42. The diclofop-methyl-resistant AR1 accession was susceptible, i.e., not cross resistant, to both aryloxyphenoxypropionate herbicides, fenoxaprop-P and clodinafop, and cyclohexanedione herbicides, sethoxydim, clethodim and tralkoxydim. Diclofop similarly inhibited the acetyl-CoA carboxylase from the AR1 ( I 50=31 μM) and AHS2 ( I 50=35 μM) accessions. Absorption of [ 14 C ]diclofop-methyl was similar for the two accessions for at least the first 12 h after treatment (HAT), but was greater by the AHS2 than the AR1 accession at 24, 72, and 168 HAT. Metabolism of [ 14 C ]diclofop-methyl to diclofop was similar in AR1 and AHS2 wild oat at 24 and 72 HAT. Therefore, the mechanism of resistance to diclofop-methyl in the AR1 wild oat accession is not due to an altered ACCase enzyme nor due to differential metabolic activation of diclofop-methyl to diclofop. Difference in the pattern of absorption of [ 14 C ]diclofop-methyl between AR1 and AHS2 accessions may have a minor role. The role of other possible mechanisms of resistance is discussed.