Enhanced activity of glutathione S ‐transferases and other metabolic genes confer resistance to S ‐metolachlor in Abutilon theophrasti Medic

BACKGROUND: The long-term application of herbicides has led to the emergence of resistance, which significantly undermines the efficacy of weed control. Abutilon theophrasti Medic is a problematic weed in agricultural fields and poses an increasing threat to corn yield security in northern China. Previously, we found a population of Abutilon theophrasti had evolved resistance to S-metolachlor; however, the mechanism underlying this resistance remained unclear. RESULTS: In this study, the glutathione S-transferases (GSTs) and other metabolic genes that play a role in the herbicide resistance mechanisms of the Abutilon theophrasti population were investigated. The results indicated that the population (JL-10) exhibited a high resistance level to S-metolachlor. It also exhibited a significant cross-resistance to acetochlor, another very-long-chain fatty acid (VLCFA) inhibitor. Sensitivity to S-metolachlor was reestablished in JL-10 after the application of glutathione S-transferase inhibitor 4-chloro-7-nitrobenzofurazan (NBD-Cl). High-performance liquid chromatography-quadrupole time-of-flight-mass spectrometry (HPLC-Q-TOF-MS) detected that the metabolic efficiency of the resistant (R) population (JL-10) to S-metolachlor was higher than the susceptible (S) population (JL-9). In addition, the activities of GSTs in R population were elevated in comparison to those in S population. Subsequently, ten candidate genes associated with non-target-site resistance (NTSR), including two GSTs, three UDP-glucuronosyltransferases (UGTs), two ATP binding cassette (ABC) transporters, and three stress-resistance-related genes, were identified through RNA-sequencing and validated using quantitative polymerase chain reaction (qPCR). CONCLUSION: GSTs and other metabolic genes reduce the sensitivity of Abutilon theophrasti to S-metolachlor by enhancing metabolism and altering herbicide detoxification. Leveraging these resistance mechanisms, future development of novel regulators or combination formulations could improve herbicidal efficacy while delaying resistance evolution. © 2025 Society of Chemical Industry.