This project highlights one component of a broader portfolio of center-funded research initiatives focused on developing novel approaches to complex scientific challenges.

Annual bluegrass (Poa annua L.) is one of the most common and problematic weeds in managed turfgrass, and repeated use of herbicides with the same mechanism of action has increased selection pressure for resistant populations. Herbicide-resistant annual bluegrass reduces the reliability of available control options and complicates long-term herbicide efficacy and stewardship. This funded research evaluated annual bluegrass populations collected across North Carolina to characterize resistance to commonly used herbicides and determine whether nontarget-site resistance mechanisms contributed to reduced control. The objectives were to: 1) characterize annual bluegrass resistance to common herbicides in North Carolina turfgrass systems, and 2) evaluate potential non-target-site resistance mechanisms in selected resistant populations. Populations were collected from golf courses, athletic fields, home lawns, and other managed turfgrass sites. Initial mechanism-of-action screenings were conducted using ALS-, PSII-, and EPSPS-inhibiting herbicides. Populations showing reduced control were further evaluated in dose-response experiments, and selected resistant populations were assessed for herbicide absorption and translocation using radiolabeled herbicides.

Results confirmed that herbicide-resistant annual bluegrass is present across multiple turfgrass use sites and herbicide mechanisms of action in North Carolina. Dose-response experiments identified resistance to simazine (Princep, among others), trifloxysulfuron (Monument), and glyphosate (Roundup, among others), with resistance varying by population and mechanism of action. Compared with susceptible populations, resistant populations required higher herbicide rates to reach the same modeled 50% response level, resulting in R/S ratios as high as 15-fold for simazine, 110-fold for trifloxysulfuron, and 181-fold for glyphosate. These ratios demonstrate substantial reductions in herbicide sensitivity, relative to one another, but they should be distinguished from the product rates required to achieve high levels of control in the field. For simazine, dose-response curves showed that several resistant populations were not fully controlled even at rates exceeding 10 times the labeled rate, indicating that increasing the application rate alone would not provide acceptable annual bluegrass control in those populations (Figures 1 and 2). Annual bluegrass resistance was identified across golf courses, athletic fields, and home lawns. Mechanistic studies indicated that reduced herbicide absorption was not a primary contributor to resistance in the North Carolina populations evaluated. Reduced absorption of radiolabeled trifloxysulfuron was not detected in the ALS-resistant population, suggesting resistance was more likely associated with target-site mutation. Similarly, reduced absorption of radiolabeled glyphosate was not observed in the evaluated EPSPS-resistant population. Genotyping identified target-site mutations associated with resistance in selected populations.

Collectively, these findings support rotating herbicide mechanisms of action, using integrated weed management strategies, avoiding repeated reliance on the same herbicide programs, and monitoring control failures early. These practices are especially important because few new herbicides are currently available for turfgrass systems, and few additional options are expected in the near term. Future research should evaluate the effectiveness of integrated weed management programs across sites with confirmed resistant populations to identify strategies that maintain long-term control.