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The Mechanism of Resistance to Aryloxyphenoxypropionate and Cyclohexanedione Herbicides in a Johnsongrass Biotype

Kevin W. Bradley, Jingrui Wu, Kriton K. Hatzios and Edward S. Hagood, Jr.
Weed Science
Vol. 49, No. 4 (Jul. - Aug., 2001), pp. 477-484
Stable URL: http://www.jstor.org/stable/4046479
Page Count: 8
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Since scans are not currently available to screen readers, please contact JSTOR User Support for access. We'll provide a PDF copy for your screen reader.
The Mechanism of Resistance to Aryloxyphenoxypropionate and Cyclohexanedione Herbicides in a Johnsongrass Biotype
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Abstract

Acetyl-coenzyme A carboxylase (ACCase) assays and absorption, translocation, and metabolism experiments were conducted to investigate the mechanism(s) responsible for resistance in a johnsongrass biotype that exhibited low levels of resistance to the cyclohexanedione (CHD) herbicide sethoxydim and the aryloxyphenoxypropionate (APP) herbicides quizalofop-P and fluazifop-P. The rate of [¹⁴C]quizalofop-ethyl absorption was significantly higher in the resistant compared to the susceptible biotype 8, 24, and 48 h after treatment (HAT), but by 72 HAT, there was no significant difference in the amount of [¹⁴C]quizalofop-ethyl detected in either biotype. Additionally, little or no differences in the translocation of [¹⁴C]quizalofop-ethyl were observed in the resistant and susceptible biotypes at any time interval after application. In [¹⁴C]quizalofop-ethyl metabolism experiments, similar levels of quizalofop-ethyl and quizalofop metabolites were observed in the resistant and susceptible biotypes 8, 24, 48, and 72 HAT, but slightly higher levels of quizalofop acid were detected in the resistant biotype 48 and 72 HAT. In ACCase assays, the concentrations of quizalofop-P, clethodim, and sethoxydim that inhibited ACCase activity by 50% (I₅₀) were statistically similar in the two biotypes, indicating that the resistant johnsongrass biotype contains an ACCase that is sensitive to the APP and CHD herbicides. In the absence of APP or CHD herbicides, however, the specific activity of ACCase in the resistant biotype was two to three times greater than that of the susceptible biotype. The specific activity of ACCase in the resistant biotype was also significantly greater than that of the susceptible biotype in the presence of all concentrations of quizalofop-P and sethoxydim and in the presence of 0.1, 1, and 10 μM clethodim. These results suggest that resistance to quizalofop-P and sethoxydim is conferred by an overproduction of ACCase in the resistant johnsongrass biotype.

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