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Article Abstract
Cytochrome oxidase (Cox) is a crucial terminal oxidase in the electron transport chain. In this study, we generated 14 Cox gene deletion or overexpression mutants in . Fungicide sensitivity tests revealed that 11 Cox gene deletion mutants displayed resistance to pyraclostrobin, while 10 overexpression mutants showed hypersensitivity. RNA-Seq and RT-qPCR analyses demonstrated the upregulation of (alternative oxidase in ), 2, and 5 (alternative oxidase deficiency in ) in ΔFgCox4-2 and ΔFgCox17-75 mutants. In 11 Cox gene deletion mutants, expression was significantly upregulated, whereas in 10 Cox gene overexpression mutants, it was significantly downregulated. overexpression mutants exhibit resistance to pyraclostrobin, while deletion mutants show hypersensitivity to pyraclostrobin. FgAod2 and FgAod5 were identified as transcription factors for . Our findings reveal that influences pyraclostrobin sensitivity by regulating through FgAod2 and FgAod5. Understanding pyraclostrobin resistance mechanisms in could help develop better fungicide rotation and application strategies to manage resistance and guide the creation of new fungicides targeting different pathways.
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