Quinclorac (3,7-dichloro-quinoline-carboxylic acid) is a pre and post emergence herbicide widely used to control grass weeds (Echinochloa spp., Digitaria spp., Setaria spp.) and some broadleaf species in rice and turf. Late watergrass (Echinochloa phyllopogon (Stapf) Koss.) is one of the most noxious weeds in California rice fields. It has evolved resistance (R) to multiple herbicides with different modes of action. A late watergrass biotype resistant to quinclorac has been found in a rice field of the Sacramento valley where quinclorac has never been applied. We characterized quinclorac resistance in this biotype and investigated the mechanism. Ratios (R/S) of the GR50 values ranged from 6 to 18 when quinclorac was applied as a foliar spray or hydroponically, respectively. Quinclorac stimulated rapid (6 HAT) ethylene formation and S plants produced 3.1 times more ethylene than R plants. Pre-treatment with malathion (a cytochrome P450 monooxygenases inhibitor) prior to quinclorac application, increased ethylene formation in S plants by 7.6 fold compared to R plants, while no such increase in ethylene formation was observed in R plants pretreated with malathion. Despite this lack of ethylene stimulation in malathion pre-treated R plants, malathion enhanced quinclorac reduction of chlorophyll fluorescence (Fv/Fm) and total biomass in both biotypes; thus in presence of the inhibitor, R plants became as susceptible to quinclorac as S plants. Quinclorac-induced reduction of late watergrass biomass was accompanied by a similar damage to photosynthetic integrity (reduction in Fv/Fm) in leaves, perhaps related to HCN release during ethylene biosynthesis in quinclorac-treated plants. However, since malathion synergism of quinclorac toxicity (enhanced fresh weight and Fv/Fm reduction) was not observed with respect to ethylene production, it is possible that quinclorac toxicity may also involve an additional mechanism causing photosynthetic damage, besides one hypothetically related to ethylene and HCN. These data suggest that resistance to quinclorac in the R late watergrass biotype involved two mechanisms: a) enhanced P450 detoxification of either quinclorac or a quinclorac-induced toxicants; b) Insensitivity along the response pathway whereby quinclorac induces ethylene production (“target site resistance”). This adds new mechanisms of resistance to those already reported for this multiple-herbicide-resistant biotype that has already spread throughout most of the CA rice fields. Pre-existing resistance to quinclorac further complicates management of herbicide-resistant E. phyllopogon in rice.
Quinclorac resistance in California's late watergrass (Echinochloa phyllopogon (Stapf.) Koss.)
MILAN, MARCO;
2009-01-01
Abstract
Quinclorac (3,7-dichloro-quinoline-carboxylic acid) is a pre and post emergence herbicide widely used to control grass weeds (Echinochloa spp., Digitaria spp., Setaria spp.) and some broadleaf species in rice and turf. Late watergrass (Echinochloa phyllopogon (Stapf) Koss.) is one of the most noxious weeds in California rice fields. It has evolved resistance (R) to multiple herbicides with different modes of action. A late watergrass biotype resistant to quinclorac has been found in a rice field of the Sacramento valley where quinclorac has never been applied. We characterized quinclorac resistance in this biotype and investigated the mechanism. Ratios (R/S) of the GR50 values ranged from 6 to 18 when quinclorac was applied as a foliar spray or hydroponically, respectively. Quinclorac stimulated rapid (6 HAT) ethylene formation and S plants produced 3.1 times more ethylene than R plants. Pre-treatment with malathion (a cytochrome P450 monooxygenases inhibitor) prior to quinclorac application, increased ethylene formation in S plants by 7.6 fold compared to R plants, while no such increase in ethylene formation was observed in R plants pretreated with malathion. Despite this lack of ethylene stimulation in malathion pre-treated R plants, malathion enhanced quinclorac reduction of chlorophyll fluorescence (Fv/Fm) and total biomass in both biotypes; thus in presence of the inhibitor, R plants became as susceptible to quinclorac as S plants. Quinclorac-induced reduction of late watergrass biomass was accompanied by a similar damage to photosynthetic integrity (reduction in Fv/Fm) in leaves, perhaps related to HCN release during ethylene biosynthesis in quinclorac-treated plants. However, since malathion synergism of quinclorac toxicity (enhanced fresh weight and Fv/Fm reduction) was not observed with respect to ethylene production, it is possible that quinclorac toxicity may also involve an additional mechanism causing photosynthetic damage, besides one hypothetically related to ethylene and HCN. These data suggest that resistance to quinclorac in the R late watergrass biotype involved two mechanisms: a) enhanced P450 detoxification of either quinclorac or a quinclorac-induced toxicants; b) Insensitivity along the response pathway whereby quinclorac induces ethylene production (“target site resistance”). This adds new mechanisms of resistance to those already reported for this multiple-herbicide-resistant biotype that has already spread throughout most of the CA rice fields. Pre-existing resistance to quinclorac further complicates management of herbicide-resistant E. phyllopogon in rice.
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