What question did this study set out to answer?

This research aims to understand the mechanisms behind ALS inhibitor resistance in blackgrass populations.

July 26, 2026Weed Technology0 citationsOpen Access

Characterization of ALS Inhibitor Resistance in Alopecurus myosuroides : Primary Role of Trp574Leu and Secondary Contributions of Additional Mutations and Metabolism

MFMujeeba FidaAnhui University of Science and Technology RCRui ChengChinese Academy of Sciences MWMengjie WangNanjing University of Chinese Medicine

Key Points

This research aims to understand the mechanisms behind ALS inhibitor resistance in blackgrass populations.
Field populations were screened for herbicide resistance, selecting R-06 and S-19 for detailed study.
ALS gene sequencing and molecular docking analyses were used to identify amino acid substitutions and binding alterations.
Metabolic inhibitor assays and GST activity assays were performed to explore herbicide sensitivity and resistance mechanisms.
The R-06 population displayed a primary resistance mechanism linked to the Trp574Leu mutation, identified alongside Pro232Thr and His363Lys mutations.
Molecular docking suggested that the binding of mesosulfuron-methyl was altered in the mutant ALS model.
GST activity was higher in the R-06 population, indicating a possible increase in metabolic resistance.

Abstract

Abstract Blackgrass is a highly competitive weed in wheat fields and has increasingly evolved resistance to acetolactate synthase (ALS)-inhibiting herbicides. Ten field populations were screened, resulting in the selection of one highly resistant population (R-06) and one susceptible population (S-19) for detailed study. Whole-plant bioassays, ALS gene sequencing, molecular docking, metabolic inhibitor assays, glutathione S-transferase (GST) and ALS activity assays, and cross-resistance profiling were conducted to dissect the mechanisms of resistance. ALS sequencing identified three amino acid substitutions in R-06: Pro232Thr (P232T), His363Lys (H363K), and Trp574Leu (W574L). While W574L is a well-characterized ALS resistance-conferring mutation, P232T and H363K are outside major resistance hotspots and may serve secondary or compensatory roles. Molecular docking analyses predicted altered binding of mesosulfuron-methyl in the mutant ALS model, consistent with structural changes in the binding pocket. Metabolic inhibitor assays using malathion, piperonyl butoxide (PBO), and NBD-Cl resulted in modest increases in herbicide sensitivity, with a maximum reduction factor of 2.95 for PBO. GST activity was higher in R-06 at a single sampling time point (3 DAT). In addition, R-06 showed reduced sensitivity to several ALS inhibitors and reduced efficacy against selected herbicides with alternative modes of action. High-level resistance to mesosulfuron-methyl in the R-06 population is primarily associated with the ALS target-site mutation Trp574Leu, while the roles of Pro232Thr, His363Lys, and metabolism appear secondary and remain unresolved. These findings highlight complex resistance patterns in blackgrass and emphasize the need for diversified and integrated weed management strategies.

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