Succinate Dehydrogenase Subunits Differentially Regulate Physiology, SDHI Sensitivity, and DON Biosynthesis in Fusarium pseudograminearum

Fusarium pseudograminearum causes wheat Fusarium crown rot, including substantial yield losses and mycotoxin contamination. Despite numerous succinate dehydrogenase inhibitors (SDHIs) being developed, most display limited efficacy against Fusarium spp., and their target Sdh subunit’s function remains incompletely understood. We systematically characterized five FpSdh genes via gene deletion and phenotypic analysis. Deletion of FpSdhA / B / D, or both FpSdhC 1 / C 2, impaired mycelial growth, conidiation, pathogenicity, and deoxynivalenol (DON) production. Notably, single Δ FpSdhC 1 /Δ FpSdhC 2 mutants grew normally, but had opposing SDHI sensitivity: Δ FpSdhC 1 was hypersensitive to 7 SDHIs; Δ FpSdhC 2 exhibited reduced sensitivity to 8 fungicides. Moreover, Δ FpSdhC 2 also decreased DON production and toxisomes abundance, highlighting its crucial role in DON biosynthesis. FpSdhC 1 was upregulated in other FpSdhs deletion mutants. Collectively, FpSdhA / B/D are crucial for core physiology, FpSdhC 1 determines intrinsic SDHIs resistance, and FpSdhC 2 is essential for DON biosynthesis. The investigation provides crucial insights into SDHI sensitivity, aiding next-generation fungicides against Fusarium diseases and mycotoxin risk.