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

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.