Metabolic resistance to S‐metolachlor in two waterhemp (Amaranthus tuberculatus) populations from Illinois, USA

BACKGROUND Two waterhemp (Amaranthus tuberculatus) populations from Illinois demonstrating multiple‐resistance to acetolactate synthase (ALS)‐, 4‐hydroxyphenylpyruvate dioxygenase, and photosystem II (PSII)‐inhibiting herbicides (designated CHR and SIR) also displayed reduced sensitivity to very‐long‐chain fatty acid‐inhibiting herbicides, including S‐metolachlor. We hypothesized that a physiological mechanism, such as enhanced metabolism, could be responsible for the reduced efficacy of S‐metolachlor. RESULTS Metabolism experiments indicated that resistant populations degraded S‐metolachlor more rapidly than sensitive populations and equally as rapidly as corn 2–24 h after treatment (HAT). Resistant waterhemp and corn metabolized 90% (DT90) of absorbed S‐metolachlor in less than 3.2 h whereas DT90 values for sensitive waterhemp exceeded 6 h. The glutathione S‐transferase inhibitor 4‐chloro‐7‐nitrobenzofurazon and cytochrome P450‐inhibitor malathion decreased the amount of S‐metolachlor metabolized in resistant waterhemp at 4 HAT but not in sensitive waterhemp or corn, and altered the abundance of certain metabolites in resistant waterhemp. CONCLUSION Results from this research demonstrate that resistance to S‐metolachlor in these waterhemp populations is due to enhanced herbicide metabolism relative to sensitive populations. In addition, our results indicate that resistant waterhemp might utilize metabolic pathway(s) more intricate than either sensitive waterhemp or corn based on their metabolite profiles. © 2020 Society of Chemical Industry Resistance to S‐metolachlor in two Amaranthus tuberculatus populations is due to enhanced metabolism. This is the first reported resistance mechanism to S‐metolachlor in a dicot weed species.