The mitotic-inhibiting herbicide pronamide controls susceptible annual bluegrass (Poa annua L.) pre- and post-emergence, but in some resistant populations, post-emergence 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 was 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 (Thr239-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 3–13% 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, 24, 72, and 168 HAT, 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 (MOA), and one of which is resistant to three MOA. 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 Thr239-Ile mutation of the α-tubulin gene.

Annual bluegrass (Poa annua L.) is a problematic weed in turfgrass that has evolved resistance to 12 different herbicide sites of action. The mitotic inhibiting herbicide pronamide has both pre-and postemergence activity on susceptible annual bluegrass populations, but on certain resistant populations, postemergence activity is hypothetically compromised due to lack of root uptake or due to an unknown foliar resistance mechanism. Spray droplet size may affect foliar and soil deposition of pronamide, thus potentially explaining variation in population control or differential shoot and root uptake. Greenhouse experiments were conducted to quantify pronamide, flazasulfuron, and pronamide + flazasulfuron (a common tank mixture) deposition on annual bluegrass as affected by spray-droplet size. Five droplet sizes (200, 400, 600, 800, and 1,000 μm) were sprayed in an enclosed spray chamber on two-to three-leaf stage annual bluegrass plants. Fluorescent dye was added to each treatment solution to quantify the effects of herbicide and spray droplet size on herbicide deposition. Results indicate that spray droplet size affects deposition of pronamide and flazasulfuron, applied alone and in combination, on annual bluegrass. The highest foliar deposition was produced with 400-μm spray droplets in pronamide treatments and with 200 μm spray droplets in flazasulfuron and pronamide + flazasulfuron treatments. The addition of flazasulfuron to pronamide did not affect herbicide deposition when compared with pronamide-alone treatments. Results suggest that 200-to 400-μm spray droplets are optimal for foliar deposition of pronamide. Alternatively, larger droplet sizes may facilitate better soil deposition of pronamide where root uptake is optimal.