Negatively Regulates Virulence via Enhancing Effector Expression and Suppressing Host Immune Responses.

The soil-borne fungal pathogen causes devastating vascular wilt disease in numerous crops, including cotton. In this study, we reveal that , a highly conserved sarcosine oxidase gene, is significantly upregulated during host infection and plays a multifaceted role in fungal physiology and pathogenicity. Functional deletion of leads to increased fungal virulence, accompanied by enhanced microsclerotia formation, elevated carbon source utilization, and pronounced upregulation of effector genes, including over 50 predicted secreted proteins genes. Moreover, the knockout strains suppress the expression of key defense-related transcription factors in cotton, such as WRKY, MYB, AP2/ERF, and GRAS families, thereby impairing host immune responses. Transcriptomic analyses confirm that orchestrates a broad metabolic reprogramming that links nutrient acquisition to immune evasion. Our findings identify as a central regulator that promotes virulence by upregulating effector gene expression and suppressing host immune responses, offering novel insights into the molecular basis of host-pathogen interactions and highlighting potential targets for disease management.