Alternative Splicing Isoforms of FgSdhC 1 Differentially Modulate Intrinsic SDHI Resistance and Biological Fitness in Fusarium graminearum

Abstract Alternative splicing (AS) of FgSdhC1 was identified in SDHI-sensitive (FgS) and intrinsically resistant (FgR) Fusarium graminearum isolates, generating four AS isoforms in each background. Isogenic replacement assays showed that individual isoforms differentially altered sensitivity to pydiflumetofen, boscalid, and fluopyram and affected multiple fitness-related traits. The average compound fitness index of FgR-derived isoform replacement strains was 0.54, compared with 0.20 for FgS-derived strains, and FgRAD2-C showed the highest value (1.43). FgSIR and FgSAD3 transcripts were significantly more abundant in FgS-C than the corresponding FgR-derived isoforms in FgR-C. Isoform transcript abundance, SDH activity, carbon source utilization, and responses to environmental stresses also differed among replacement strains. Transcriptomic and RT-qPCR analyses identified FgPRPF4B, FgDHX38/FgPRP16, and FgPPIL1 as differentially expressed candidate splicing-related genes. Collectively, these findings showed that FgSdhC1 alternative splicing isoforms differentially modulate intrinsic SDHI resistance and biological fitness in F. graminearum.