Regulation of FpvelC on Conidiation, Pathogenicity and Secondary Metabolism in Fusarium proliferatum

The velvet complex is a master regulator of multiple physiological processes in filamentous fungi. In this study, we characterized the functions of velvet gene <i>FpvelC</i> in <i>Fusarium proliferatum</i>, which was the causative agent of rice spikelet rot disease. Compared with the wild-type Fp9 strain, deletion of <i>FpvelC</i> hindered conidiation, leading to a low level of trehalose content but excessive accumulation of chitin in conidia. Lack of <i>FpvelC</i> resulted in increased sensitivity to oxidative stress and decreased expression of antioxidant genes. Notably, Δ<i>FpvelC</i> exhibited attenuated pathogenicity on rice and maize, failure to produce invasive hyphae, and downregulation of genes encoding xylanases and xyloglucanases during infection processes. Nevertheless, disruption of <i>FpvelC</i> enhanced production of fumonisin B1 (FB1) and fusaric acid concomitantly; transcripts of the clustering genes responsible for the two mycotoxins' biosynthesis were significantly increased. Additionally, the absence of <i>FpvelC</i> was displayed as more sensitive to rapamycin than the Fp9 strain, accompanied with less intracellular glutamine. Overall, <i>FpvelC</i> played versatile roles in conidiation, response to oxidative stress, pathogenicity and mycotoxins production in <i>F. proliferatum</i>.