Submitted to: International Weed Control Congress Proceedings
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 6/24/1996
Publication Date: N/A
Citation: Interpretive Summary: In 1990 and 1991 Farmers in the Willamette Valley of Oregon found that diclofop, a herbicide that has been used to control wild oat in wheat and other crops for over ten years, was no longer effective. Researchers in Oregon determined that these wild oat plants were resistant to diclofop. In greenhouse studies conducted on wild oat from 8 of these farms (8 biotypes), levels of resistance to diclofop varied from 3 to 64 times greater than a susceptible wild oat. Diclofop and some other herbicides kill by inhibiting the enzyme acetyl CoA carboxylase. Many of the wild oat biotypes were resistant to these related herbicides. These biotypes often had very different characteristics (e.g. short, tall, bushy) which indicates that these biotypes were not related and that the resistance trait was selected for independently in each of these fields. Laboratory studies found that resistance in two of the wild oat biotypes was due to an naltered acetyl CoA carboxylase enzyme. Genetic studies in the greenhouse show that the resistance is due primarily to a single gene that, at normal field rates of diclofop, could be considered dominant. Because these resistant biotypes were selected for independently, one can assume that more cases of diclofop-resistance will occur wherever diclofop is used. The resistance to other, related herbicides means that these herbicides will not be available to control the diclofop-resistant wild oat. It will be difficult to develop a new herbicide that can target the acetyl CoA carboxylase enzyme as apparently there are several resistant forms. The single gene nature of the resistance trait makes the spread of the resistance trait much easier than would a multiple gene trait. Diclofop- resistant wild oat could become a major problem in agriculture.
Technical Abstract: Diclofop-resistant Avena fatua was found in the Willamette Valley of Oregon. Multiple applications of diclofop over a ten year period provided selection pressure for resistance in these fields. These biotypes differed widely in morphological traits suggesting they originated independently. There were large differences in both the levels of resistance to diclofop and the patterns of cross-resistance to other aryloxyphenoxypropionate and cyclohexanedione herbicides, suggesting a different basis for resistance among the Avena fatua from the 10 fields. Mechanism of resistance studies suggested that changes in the site of action (acetyl CoA carboxylase) were largely responsible for the resistance. There were small differences in absorption, translocation and metabolism of diclofop, but, if anything, these all tended to be in the direction making the resistant biotypes more susceptible. Inheritance of the resistance trait suggested that resistance ewas due to a single, partially dominant gene with a possible modifying genetic factor that reduced resistance to high doses of diclofop.