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Annual bluegrass is a troublesome weed in turfgrass, with reported resistance to at least 12 herbicide sites of action. The mitotic-inhibiting herbicide pronamide has both preemergence and postemergence activity on susceptible annual bluegrass populations. Previous studies suggest that postemergence activity may be compromised due to lack of root uptake, as well as target-site- and translocation-based mechanisms. Research was conducted to determine the effects of spray droplet spectra on spray coverage and control of annual bluegrass with pronamide, flazasulfuron, and a mixture of pronamide plus flazasulfuron. Herbicides were delivered to annual bluegrass plants having two to three leaves via five different spray spectra based on volume median diameters (VMD) of 200, 400, 600, 800, and 1,000 µm. Fluorescent tracer dye was added to each treatment solution to quantify the effects of herbicide and spray droplet spectra on herbicide deposition. In another experiment, the efficacy of 0.58, 1.16, and 2.32 kg pronamide ha−1; 0.022, 0.044, and 0.088 kg flazasulfuron ha−1, or a combination of the two, were assessed in iteration with droplet spectrum sprays of 400 and 1,000 µm on two pronamide-resistant and two pronamide-susceptible annual bluegrass populations. Spray droplet spectrum affected the deposition of pronamide and flazasulfuron, applied alone and in combination. Pronamide foliar deposition decreased with increasing droplet spectra. Pronamide efficacy was affected by droplet spectrum, with the largest (1,000 µm) exhibiting improved control. Flazasulfuron efficacy and pronamide plus flazasulfuron efficacy were not affected by droplet spectra. Pronamide plus flazasulfuron mixture controlled all four populations more effectively than pronamide alone, regardless of droplet spectra. A mixture of pronamide plus flazasulfuron applied with relatively large droplets may be optimal for annual bluegrass control, which offers valuable insights for optimizing herbicide application and combatting herbicide resistance. However, applications in this controlled-growth pot study may not mimic conditions in which thatch and turfgrass canopy limit the soil deposition of pronamide.
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.
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