Non-target-site mechanisms of cross-resistance evolution to florpyrauxifen-benzyl in 2,4-D-resistant Palmer amaranth (Amaranthus palmeri)

Abstract

ABSTRACT The evolution of herbicide resistance in weeds can reduce the herbicides efficacy, depleting crop yield and quality. Our group previously confirmed 2,4-D resistance in three Palmer amaranth (Amaranthus palmeri S. Watson) populations (R13). In the current study, the first filial (F1) seeds of 2,4-D-resitant populations were subjected to resistance screening tests to other auxin-mimicking herbicides, florpyrauxifen-benzyl (FPB; 30 g ai ha-1) and dicamba (560 g ae ha-1). Dicamba killed all resistant populations. FPB provided 100% control of only the R3 population. Sensitivities to FPB were reduced by 2 and 35 percentage points in R1 and R2 populations, respectively. Pre-treatment with malathion increased FPB sensitivity by 15 percentage points in the R2 population. FPB resistance characterization and mechanism were evaluated using a purified line of the R2 population (F2). The FPB sensitivity was 29-fold lower in the F2 line than in the susceptible (S) standard. Absorption, translocation, and total metabolism of FPB were similar for S and R2 populations. However, less florpyrauxifen-acid (FPA) was detected in the R2 population (17.0% to 25.4%) than in the S population (22.8% to 33.2%), due to its rapid metabolism and/or reduced production with resistance evolution. Since the results of the non-target-site resistance mechanism evaluation observed in this study were insufficient to account for the 29-fold reduced sensitivity of the R2 population to FPB, further genetic studies are needed to investigate the presence of target-site resistance in that population.