Fusarium oxysporum f. sp. cubense (Foc), the causal agent of banana Fusarium wilt, is one of the most destructive plant pathogens worldwide. However, the molecular mechanisms that integrate fungal growth, metabolism, and virulence remain poorly understood. This study identifies and functionally characterizes FoSrk1, a serine/arginine-rich protein kinase (SRPK), in Foc. Deletion of FoSrk1 markedly impaired vegetative growth, reduced aerial mycelium formation and conidiation, and significantly attenuated virulence toward banana plantlets. The mutant also exhibited compromised utilization of diverse carbon sources, accompanied by altered expression of 32 genes involved in carbon metabolism. Complementation with the wild-type FoSrk1 allele restored normal growth and pathogenicity, confirming the gene’s essential role. Transcriptomic analyses revealed that loss of FoSrk1 altered the expression of 2,500 genes and was associated with changes in 37 alternative splicing events, predominantly intron retention, affecting transcripts linked to protein metabolism, ribosome biogenesis, and redox processes. Moreover, several virulence-associated genes encoding ABC transporters, cytochrome P450 enzymes, and hydrophobins were downregulated in the FoSrk1-deficient strain. These findings suggest that FoSrk1 acts as an important regulator that couples RNA processing with metabolic and pathogenic pathways and is required for normal fungal development and virulence. This study provides new insight into the molecular basis of pathogenic adaptation and identifies FoSrk1 as a potential target for antifungal intervention strategies.
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