In Arkansas, resistance to protoporphyrinogen IX oxidase (PPO)-inhibiting herbicides in Amaranthus palmeri S. Wats. is mainly due to target site mutations. Although A. palmeri PPO-mutations are well investigated, the cross-resistance that each ppo mutant endows to weed populations is not yet well understood. We aimed to evaluate the response of PPO-resistant A. palmeri accessions, harboring the ppo2 mutations ΔG210 and G399A, to multiple PPO-inhibiting herbicides. Six resistant and one susceptible field accessions were subjected to a dose–response assay with fomesafen, and selected survivors from different fomesafen doses were genotyped to characterize the mutation profile. The level of resistance to fomesafen was determined and a cross-resistance assay was conducted with 1 and 2 times the labeled doses of selected PPO herbicides. The accession with higher predicted dose to control 50% of the population (ED50) had a higher frequency of ΔG210-homozygous survivors. Survivors harboring both mutations, and those that were ΔG210-homozygous, incurred less injury at the highest fomesafen rate tested (1120 g ai ha−1). The populations with a high frequency of ΔG210-homozygous survivors, and those with individuals harboring ΔG210 + G399A mutations, exhibited high potential for cross-resistance to other PPO herbicides. The new PPO–herbicide chemistries (saflufenacil, trifludimoxazin) generally controlled the PPO-resistant populations.
The cross-resistance patterns and biochemical characteristics of an imidacloprid-resistant strain of the cotton aphid
