Abstract

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 FpSdhC1/C2, impaired mycelial growth, conidiation, pathogenicity, and deoxynivalenol (DON) production. Notably, single ΔFpSdhC1/ΔFpSdhC2 mutants grew normally, but had opposing SDHI sensitivity: ΔFpSdhC1 was hypersensitive to 7 SDHIs; ΔFpSdhC2 exhibited reduced sensitivity to 8 fungicides. Moreover, ΔFpSdhC2 also decreased DON production and toxisomes abundance, highlighting its crucial role in DON biosynthesis. FpSdhC1 was upregulated in other FpSdhs deletion mutants. Collectively, FpSdhA/B/D are crucial for core physiology, FpSdhC1 determines intrinsic SDHIs resistance, and FpSdhC2 is essential for DON biosynthesis. The investigation provides crucial insights into SDHI sensitivity, aiding next-generation fungicides against Fusarium diseases and mycotoxin risk.