Submitted to: Weed Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 3/22/1996
Publication Date: N/A
Citation: Interpretive Summary: In 1990, wild oat resistant to diclofop were found in two different fields in Oregon. Herbicides, especially diclofop, have controlled wild oat effectively in the past. This research was designed to find out why the wild oat plants were resistant which could lead to a new control method. Wild oat in one field was also resistant to fenoxaprop, a herbicide with a mode of action similar to diclofop. Acetyl CoA carboxylase, the enzyme to which diclofop binds, was not inhibited as much in the resistant wild oat compared to the susceptible wild oat. A similar response was observed with fenoxaprop. These results show that there are multiple types of changes that can occur to the acetyl CoA carboxylase enzyme that would make a herbicide-susceptible wild oat resistant. This plasticity will make it more difficult to develop chemical control methods that target acetyl CoA carboxylase. In fields where resistance to diclofop occurs, it is important that the grower stop using diclofop and any other herbicide related to diclofop and take measures to prevent the spread of the seed from the resistant plants. Before the advent of wild oat herbicides 15 to 20 years ago, wild oat was one of the worst weeds in agriculture, costing growers in North America over 1 billion dollars a year. If a solution to herbicide resistant wild oat is not developed, wild oat may well reemerge as one of the most troublesome weeds.
Technical Abstract: Laboratory experiments were conducted to determine the mechanism of resistance to diclofop in two wild oat biotypes (designated `B' and `C' biotypes) from the Willamette Valley of Oregon. Resistance could not be attributed to differential absorption, translocation, or metabolism of diclofop. Resistance was not correlated with membrane plasmalemma repolarization following diclofop acid treatment. Compared to a susceptible wild oat biotype (`S'), acetyl CoA carboxylase from the B and C biotypes showed a 10.3 and 4.5 fold increase in the level of resistance, respectively, to diclofop acid. Cross-resistance to fenoxaprop acid was 5.5 and 7.3 times higher in the B and C biotype, respectively than the S biotype. There was good correlation between the enzyme and whole plant resistance levels in the B biotype for both diclofop (17 fold increase) and fenoxaprop (3.4 fold increase). The correlation between the enzyme and whole plant resistance levels in the C biotype for both diclofop (23 fold increase) and fenoxaprop (47 fold increase) was not as good. Reasons for the discrepancy are given.