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Yasuor, H., Weed Science Program, Department of Plant Sciences, University of California, Davis, CA 95616, United States, Department of Plant Sciences, University of California, Mail Stop 4, One Shields Ave., Davis, CA 95616-8780, United States
TenBrook, P.L., Department of Environmental Toxicology, University of California, Davis, CA 95616, United States
Tjeerdema, R.S., Department of Environmental Toxicology, University of California, Davis, CA 95616, United States
Fischer, A.J., Weed Science Program, Department of Plant Sciences, University of California, Davis, CA 95616, United States
BACKGROUND: Late watergrass [Echinochloa phyllopogon (Stapf.) Koss.] is a major weed of Californian rice that has evolved P450-mediated metabolic resistance to multiple herbicides. Resistant (R) populations are also poorly controlled by the recently introduced herbicide clomazone. The authors assessed whether this cross-resistance was also P450 mediated, and whether R plants also had reduced sensitivity to photooxidation. Understanding mechanism(s) of resistance facilitates the design of herbicide management strategies to delay resistance evolution. RESULTS: Ratios (R/S) of R to susceptible (S) GR 50 were near 2.0. [14C]Clomazone uptake was similar in R and S plants. Clomazone and its metabolite 5-ketoclomazone reduced chlorophyll and carotenoids in S more than in R plants. The P450 inhibitors disulfoton and 1-aminobenzo-triazole (ABT) safened clomazone in R and S plants. Disulfoton safened 5-ketoclomazone only in S plants, while ABT synergized 5-ketoclomazone mostly against S plants. Paraquat was more toxic in S than in R plants. CONCLUSION: Cross-resistance to clomazone explains failures to control R plants in rice fields, and safening by P450 inhibitors suggests that oxidative activation of clomazone is needed for toxicity to E. phyllopogon. Clomazone resistance requires mitigation of 5-ketoclomazone toxicity, but P450 detoxification may not significantly confer resistance, as P450 inhibitors poorly synergized 5-ketoclopmazone in R plants. Responses to paraquat suggest research on mechanisms to mitigate photooxidation in R and S plants is needed. © 2008 Society of Chemical Industry.
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Responses to clomazone and 5-ketoclomazone by Echinochloa phyllopogon resistant to multiple herbicides in Californian rice fields
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Yasuor, H., Weed Science Program, Department of Plant Sciences, University of California, Davis, CA 95616, United States, Department of Plant Sciences, University of California, Mail Stop 4, One Shields Ave., Davis, CA 95616-8780, United States
TenBrook, P.L., Department of Environmental Toxicology, University of California, Davis, CA 95616, United States
Tjeerdema, R.S., Department of Environmental Toxicology, University of California, Davis, CA 95616, United States
Fischer, A.J., Weed Science Program, Department of Plant Sciences, University of California, Davis, CA 95616, United States
Responses to clomazone and 5-ketoclomazone by Echinochloa phyllopogon resistant to multiple herbicides in Californian rice fields
BACKGROUND: Late watergrass [Echinochloa phyllopogon (Stapf.) Koss.] is a major weed of Californian rice that has evolved P450-mediated metabolic resistance to multiple herbicides. Resistant (R) populations are also poorly controlled by the recently introduced herbicide clomazone. The authors assessed whether this cross-resistance was also P450 mediated, and whether R plants also had reduced sensitivity to photooxidation. Understanding mechanism(s) of resistance facilitates the design of herbicide management strategies to delay resistance evolution. RESULTS: Ratios (R/S) of R to susceptible (S) GR 50 were near 2.0. [14C]Clomazone uptake was similar in R and S plants. Clomazone and its metabolite 5-ketoclomazone reduced chlorophyll and carotenoids in S more than in R plants. The P450 inhibitors disulfoton and 1-aminobenzo-triazole (ABT) safened clomazone in R and S plants. Disulfoton safened 5-ketoclomazone only in S plants, while ABT synergized 5-ketoclomazone mostly against S plants. Paraquat was more toxic in S than in R plants. CONCLUSION: Cross-resistance to clomazone explains failures to control R plants in rice fields, and safening by P450 inhibitors suggests that oxidative activation of clomazone is needed for toxicity to E. phyllopogon. Clomazone resistance requires mitigation of 5-ketoclomazone toxicity, but P450 detoxification may not significantly confer resistance, as P450 inhibitors poorly synergized 5-ketoclopmazone in R plants. Responses to paraquat suggest research on mechanisms to mitigate photooxidation in R and S plants is needed. © 2008 Society of Chemical Industry.
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