Succinate dehydrogenase (Sdh) is a conserved mitochondrial complex linking the tricarboxylic acid cycle and electron transport chain and is the target of SDHI fungicides. However, the roles of individual Sdh subunits in fungal development and SDHI responses remain unclear. Here, we systematically characterized Sdh subunits in Fusarium verticillioides, the causal agent of maize ear rot. Deletion of FvSdhA, FvSdhB, or FvSdhD severely impaired fungal growth, conidiation, toxin production, pathogenicity, and concurrently reduced sensitivity to the SDHI fungicide pydiflumetofen. In contrast, the duplicated membrane-anchoring subunits FvSdhC1 and FvSdhC2 exhibited partial functional redundancy as deletion of FvSdhC1 led to a dramatic upregulation of FvSdhC2 transcript, and both could potentially support Sdh complex formation, while they exerted distinct effects on virulence and SDHI response. Together, these findings suggest functional specialization within the FvSdh complex and indicate that FvSdhC paralogs may contribute to adaptive fungicide responses through coordinated structural and transcriptional divergence.
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