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.

Poor annual bluegrass control was reported in golf course roughs following treatment with prodiamine (1120 gaiha−1) and glyphosate (840 gaeha−1) during hybrid bermudagrass dormancy. Research was conducted to determine if this annual bluegrass phenotype was resistant to both prodiamine and glyphosate and to determine the efficacy of herbicide mixtures for controlling this phenotype in the field. In PRE or POST dose-response experiments, 9 to 31 times more prodiamine or glyphosate was needed to control (or reduce dry biomass of) this resistant phenotype by 50% compared to an herbicide-susceptible phenotype. Moreover, glyphosate-susceptible plants accumulated 50% more shikimic acid (898 mgkg−1) 6 d after treatment than those resistant to glyphosate (394 mgkg−1). October (fall) applications of herbicide mixtures containing trifloxysulfuron, simazine, S-metolachlor, or mesotrione controlled this resistant annual bluegrass phenotype 84 to 98% in April (spring), with no differences detected among treatments. Our findings document the second instance of annual bluegrass evolving multiple resistance in a managed turfgrass system. However, several herbicide mixtures can be used to effectively manage this resistant phenotype.