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Mitotic-inhibiting herbicides, like prodiamine and dithiopyr, are used to control annual bluegrass (Poa annua L.) preemergence in managed turfgrass; however, resistance to mitotic-inhibiting herbicides has evolved due to repeated applications of herbicide from a single mechanism of action. Three suspected resistant populations (R1, R2, and R3) were collected in Alabama and Florida and screened for resistance to prodiamine. Part of the α-tubulin gene was sequenced for known target-site mutations. Target-site mutations were reported in all three R populations, with each containing an amino acid substitution at position 239 from threonine to isoleucine (Thr-239-Ile). Previous research has indicated that the Thr-239-Ile mutation confers resistance to dinitroaniline herbicides in other species. Dose–response screens using prodiamine and dithiopyr were conducted and I50 values were calculated for R1, R2, and R3 using regression models based on seedling emergence. For prodiamine, I50 values for R1, R2, and R3 were 35.3, 502.7, and 91.5 g ai ha−1, respectively, resulting in 2.9-, 41.9-, and 7.6-fold resistance, respectively, when compared with a susceptible (S) population. For dithiopyr, I50 values for R1, R2, and R3 were 154.0, 114.2, and 190.1 g ai ha−1, respectively, resulting in 3.6-, 2.7-, and 4.5-fold resistance, respectively, when compared with an S population. When comparing I90 values with the highest labeled use rates, R2 had a 2.9-fold level of resistance to prodiamine, and R1, R2, and R3 had a 2.4-, 2.0-, and 3.2-fold levels of resistance to dithiopyr, respectively. This is the first report of a variable response in P. annua to prodiamine despite each R population possessing the same mutation.
The goal of weed science extension efforts are to encourage and accelerate adoption of diverse, effective, and economical management tactics. To be most successful and efficient, extension personnel need to know how growers prefer to receive information, the format in which the information is delivered, and areas that future extension research should focus on. To this end, surveys were distributed at crop and forage extension meetings in Virginia. The results from 249 responses indicate that both crop and forage producers have similar preferences. Agribusiness personnel (e.g., co-ops, suppliers, vendors, crop consultants, sales representatives) had the greatest influence on herbicide-purchasing decisions and were the primary source of information for producers who make weed management decisions, and thus should be a target audience of extension. Respondents said that economic assessments, weed control data, and yield data are most likely to influence changes in their management practices and that they would prefer to receive that information through traditional extension formats (presentations, publications, and on-farm demonstrations). Generally, respondents also indicated that they wanted extension efforts to focus on evaluating new herbicides for weed control and crop safety in the future over alternative nonherbicidal weed control methods. Therefore, extension personnel are likely to be more successful by including herbicides in the practice of integrated weed management rather than relying solely on nonchemical approaches.
Dithiopyr and dinitroanilines are preemergence-applied, mitotic-inhibiting herbicides used to control goosegrass [Eleusine indica (L.) Gaertn.] in turfgrass. A suspected resistant E. indica population was collected from a golf course putting green and was evaluated for possible resistance to dithiopyr and prodiamine. After dose–response evaluation, the α-tubulin gene was sequenced for known target-site mutations that have been reported to confer resistance to mitotic-inhibiting herbicides. A mutation was discovered that resulted in an amino acid substitution at position 136 from leucine to phenylalanine (Leu-136-Phe). Previous research has indicated that Leu-136-Phe does confer resistance to dinitroaniline herbicides. The level of resistance indicated by regression models and I50 values indicates that there is 54.1-, 4.7-, >100-, and >100-fold resistance to dithiopyr, prodiamine, pendimethalin, and oryzalin, respectively, when compared with the susceptible population based on seedling emergence response and 88.4-, 7.8-, >100-, and >100-fold resistance to dithiopyr, prodiamine, pendimethalin, and oryzalin, respectively, when compared with the susceptible population based on biomass reduction response. This is the first report of less resistance to prodiamine compared with pendimethalin or oryzalin due to a target-site α-tubulin mutation and the first report of a target-site α-tubulin mutation associated with dithiopyr resistance.
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