論文信息：Tao Yin, Qiang Zhang, Jianhua Wang, Huiquan Liu, Chenfang Wang, Jin-Rong Xu and Cong Jiang. The cyclase-associated protein FgCap1 has both PKA-dependent and -independent functions during DON production and plant infection in Fusarium graminearum. Molecular Plant Pathology，2017， doi: 10.1111/mpp.12540. [Epub ahead of print]
JCR1區(qū)，IF=4.335
論文摘要：Fusarium graminearum is a causal agent of wheat scab and a producer of trichothecene mycotoxin deoxynivalenol (DON). The expression of trichothecene biosynthesis (TRI) genes and DON production are mainly regulated by the cAMP-PKA pathway and two pathway-specific transcription factors (TRI6 and TRI10). Interestingly, mutants deleted of TRI6 had reduced expression of several components of cAMP signaling, including the FgCAP1 adenylate binding protein gene that has not been functionally characterized in F. graminearum. In this study, we showed that FgCap1 interacted with Fac1 adenylate cyclase and deletion of FgCAP1 reduced the intracellular cAMP level and PKA activities. The Fgcap1 deletion mutant was defective in vegetative growth, conidiogenesis, and plant infection. It also was significantly reduced in DON production and TRI gene expression, which could be suppressed by exogenous cAMP, indicating that a PKA-dependent regulation of DON biosynthesis by FgCap1. The wild type but not tri6 mutant had increased levels of intracellular cAMP and FgCAP1 expression under DON producing conditions. Furthermore, the promoter of FgCAP1 has one putative Tri6-binding site that was important for its function during DON biosynthesis but dispensable for hyphal growth, conidiogenesis, and pathogenesis. In addition, FgCap1 has an actin-like localization to the cortical patches at the apical region of hyphal tips. Phosphorylation of FgCap1 at S353 was identified by phosphoproteomics analysis. The S353A mutation in FgCAP1 had no effects on its functions during vegetative growth, conidiation, and DON production. However, expression of the FgCAP1S353A allele failed to complement the defects of Fgcap1 mutant in plant infection, indicating the importance of phosphorylation of FgCap1 at S353 during pathogenesis. Taken together, our results suggested that FgCAP1 is involved in the regulation of DON production via cAMP signaling and subjected to a feedback regulation by TRI6, but phosphorylation of FgCap1 at S353 is likely unrelated to the cAMP-PKA pathway because S353A mutation only affected plant infection.
