Molecular Mechanisms of Resistance to Cyhalofop-Butyl in Barnyard Grass (Echinochloa crus-galli)

Cyhalofop-butyl, a widely used acetyl-CoA carboxylase (ACCase)-inhibiting herbicide, is increasingly resisted by Echinochloa crus-galli in paddy fields. However, the physiological and molecular mechanisms of this resistance have not been fully elucidated. In this study, a highly resistant population (HL-R, resistance index [RI] = 19.05) from Hulin and a susceptible population (HL-S, RI = 1.00) were used. The results showed that HL-R population exhibited broad-spectrum resistance to five herbicides (RI = 1.98–14.53). No target-site mutations were found in the ACCase gene; instead, its overexpression contributed to target-site resistance (TSR). Metabolic inhibitor assays confirmed non-target-site metabolic resistance (NTSR). Transcriptome and qRT-PCR analyses identified two detoxification-related differentially expressed genes (DEGs; CH01.636, BH02.4557) as key regulators. The activity of the antioxidant enzyme peroxidase (POD) was also associated with resistance. Collectively, the high resistance of HL-R to cyhalofop-butyl is synergistically driven by ACCase overexpression, POD activity and P450/GST-mediated metabolic detoxification. These findings provide theoretical guidance for the management of resistant barnyard grass.