Abstract
The velvet complex is a master regulator of multiple physiological processes in filamentous fungi. In this study, we characterized the functions of velvet gene FpvelC in Fusarium proliferatum, which was the causative agent of rice spikelet rot disease. Compared with the wild-type Fp9 strain, deletion of FpvelC hindered conidiation, leading to a low level of trehalose content but excessive accumulation of chitin in conidia. Lack of FpvelC resulted in increased sensitivity to oxidative stress and decreased expression of antioxidant genes. Notably, ΔFpvelC 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 FpvelC 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 FpvelC was displayed as more sensitive to rapamycin than the Fp9 strain, accompanied with less intracellular glutamine. Overall, FpvelC played versatile roles in conidiation, response to oxidative stress, pathogenicity and mycotoxins production in F. proliferatum.