Calvin G. Messersmith

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.

Altered Herbicide Target Sites

Herbicides have been important tools for weed management ever since the introduction of auxin-analog herbicides in the mid-1940s. While herbicides continue to be viable weed control options, herbicide-resistant weeds are an ever-increasing concern for world agriculture (Heap, 1997; Morrison and Devine, 1994; Shaner, 1995). Herbicide resistance is defined as the inherited ability of a plant to survive and reproduce following exposure to a dose of herbicide normally lethal to wild-type plants (Anonymous, 1998). Selection for rare resistant biotypes in weed populations is believed to be responsible for the evolution of most herbicide-resistant weed populations. Recurrent selection pressure is provided by season-after-season use of herbicides that do not control the resistant biotype(s). These herbicides are most likely those with the same or similar mode of action. Herbicide resistance has been documented in 98 dicot and 67 monocot weed species worldwide, totaling 275 species-by-mode-of-action combinations to date (Heap, 2003).