VdSOX1 Negatively Regulates Verticillium dahliae Virulence via Enhancing Effector Expression and Suppressing Host Immune Responses

The soil-borne fungal pathogen <i>Verticillium dahliae</i> causes devastating vascular wilt disease in numerous crops, including cotton. In this study, we reveal that <i>VdSOX1</i>, 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 <i>VdSOX1</i> 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 <i>VdSOX1</i> 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 <i>VdSOX1</i> orchestrates a broad metabolic reprogramming that links nutrient acquisition to immune evasion. Our findings identify <i>VdSOX1</i> as a central regulator that promotes <i>V. dahliae</i> 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.