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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 mitotic-inhibiting herbicide pronamide controls susceptible annual bluegrass (Poa annua L.) pre- and postemergence, but in some resistant populations, postemergence activity is compromised, hypothetically due to a target-site mutation, lack of root uptake, or an unknown resistance mechanism. Three suspected pronamide-resistant (LH-R, SC-R, and SL-R) and two pronamide-susceptible (BS-S and HH-S) populations were collected from Mississippi golf courses. Dose–response experiments were conducted to confirm and quantify pronamide resistance, as well as resistance to flazasulfuron and simazine. Target sites known to confer resistance to mitotic-inhibiting herbicides were sequenced, as were target sites for herbicides inhibiting acetolactate synthase (ALS) and photosystem II (PSII). Pronamide absorption and translocation were investigated following foliar and soil applications. Dose–response experiments confirmed pronamide resistance of LH-R, SC-R, and SL-R populations, as well as instances of multiple resistance to ALS- and PSII-inhibiting herbicides. Sequencing of the α-tubulin gene confirmed the presence of a mutation that substituted isoleucine for threonine at position 239 (Thr-239-Ile) in LH-R, SC-R, SL-R, and BS-S populations. Foliar application experiments failed to identify differences in pronamide absorption and translocation between the five populations, regardless of harvest time. All populations had limited basipetal translocation—only 3% to 13% of the absorbed pronamide—across harvest times. Soil application experiments revealed that pronamide translocation was similar between SC-R, SL-R, and both susceptible populations across harvest times. The LH-R population translocated less soil-applied pronamide than susceptible populations at 24, 72, and 168 h after treatment, suggesting that reduced acropetal translocation may contribute to pronamide resistance. This study reports three new pronamide-resistant populations, two of which are resistant to two modes of action (MOAs), and one of which is resistant to three MOAs. Results suggest that both target site– and translocation-based mechanisms may be associated with pronamide resistance. Further research is needed to confirm the link between pronamide resistance and the Thr-239-Ile mutation of the α-tubulin gene.
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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