Abstract
Annual bluegrass (Poa annua L.) is an annual weed that is particularly troublesome in managed turfgrass. It has been controlled conventionally with herbicides, including acetolactate synthase (ALS) inhibitors. However, resistance to ALS inhibitors has been documented throughout the southeastern United States since 2012. A rate–response trial was conducted to confirm and determine the resistance level of suspected resistant P. annua biotypes from Mississippi (Reunion), followed by DNA sequencing to determine whether the mechanism of resistance is a target-site mutatio n. In addition, a fitness assay was conducted together with a susceptible biotype to determine whether resistance to ALS inhibitors is associated with decreased fitness. Reunion was at least 45 times more resistant to foramsulfuron than the standard susceptible biotype based on I50 estimates [I50 is the rate of herbicide giving a 50% response (50% visual necrosis)], requiring a predicted 331 g a.i./ha foramsulfuron for 50% control. DNA sequencing results identified a Trp574-to-Leu mutation in the ALS gene of the Reunion biotype, which has been shown by other studies to confer resistance to ALS inhibitors. Measurement of fitness parameters among the Reunion and susceptible biotypes demonstrated reduced seed yield, tillering, and flowering time in the resistant Reunion biotype, suggesting that ALS inhibitor resistance is possibly correlated to decreased fitness in P. annua. Alternative methods to control P. annua need to be considered as a result of the evolution of herbicide-resistant biotypes. An integrated management strategy to control P. annua weeds will help prevent further evolution of resistance. Because this study evaluated only the target-site mechanism of resistance, it is also necessary to determine whether the resistant biotype has reduced uptake, translocation, or enhanced metabolism as additional mechanisms of resistance. Consequently, a fitness study encompassing a more comprehensive list of plant parameters will provide conclusions of the fitness costs associated with ALS inhibitor resistance in P. annua. Chemical names: Foramsulfuron {1-(4,6-dimethoxypyrimidin-2-yl)-3-[2-(dimethylcarbamoyl)-5-formamidophenylsulfonyl] urea}.
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