Members of Velvet Complex FpVeA and FpVelB Regulate Asexual Development, Fumonisin Biosynthesis and Virulence in Fusarium proliferatum

<i>Fusarium proliferatum</i> is the causative agent of rice spikelet rot disease, which can produce a group of toxic secondary metabolites, especially fumonisins. Velvet complex is a master regulator governing the development processes and secondary metabolism in filamentous fungi. In this study, we investigated the biological functions of velvet members FpVeA and FpVelB in <i>F. proliferatum</i>. Compared with the wild-type Fp9 strain, deletion of <i>FpveA</i> or <i>FpvelB</i> genes resulted in retarded hyphal growth but promoted conidiation. Disruption mutants exhibited decreased conidial trehalose contents and enhanced sensitivity to H₂O₂ stress, as well as inducing expression of photoreceptors. Notably, inactivation of <i>FpveA</i> or <i>FpvelB</i> led to a reduction in production of fumonisin B1 (FB1), coinciding with downregulation of fumonisin biosynthetic genes. Furthermore, the absence of <i>FpveA</i> or <i>FpvelB</i> displayed attenuated virulence toward rice spikelets, accompanied by fewer invasive hyphae and a failure of penetration ability. Taken together, these results demonstrated that FpVeA and FpVelB play crucial roles in the asexual development, oxidative stress, toxin synthesis and pathogenicity of <i>F. proliferatum</i>.