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Molecular Mechanisms of Resistance to Cyhalofop-Butyl in Barnyard Grass (Echinochloa crus-galli)
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DOI：10.3390/plants15121908.png)
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Abstract
En 中文
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.
Keywords:
cyhalofop-butyl
<i>Echinochloa crus-galli</i>
target-site resistance (TSR)
non-target-site resistance (NTSR)
transcriptomics
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4.1
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2.2W
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6.4W
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