PRJNA772019
AaStuA orchestrates environmental signals for ACT toxin biosynthesis in Alternaria alternata
The functions of an APSES transcription factor AaStuA were investigated in the tangerine pathotype of Alternaria alternata, a necrotrophic fungal pathogen that produces the host-selective toxin termed ACT (A. citri toxin). AaStuA was shown to be required for ACT biosynthesis and fungal virulence. AaStuA was found to physically interact with a pH-responsive transcription regulator AaPacC, which is also required for toxin biosynthesis and virulence. Mutation of AaStuA via targeted gene deletion or silencing AaPacC decreased the expression of seven toxin biosynthetic genes (ACCT) and toxin production. EMSA analyses revealed that AaPacC could bind to some but all of the promoters of the ACCT genes. The results confirmed that AaPacC is one of the downstream components involved in ACT biosynthesis. Moreover, experimental evidence showed that AaStuA negatively controlled autophagy via promoting the AaTor activity (target of rapamycin in A. alternata). Although AaStuA was found to be involved in ACT biosynthesis, targeted gene deletion of 19 autophagy-related genes (ATG) revealed that only some but not all ATG mutants were defective in toxin production and virulence. Whether or not autophagy directly impacts ACT biosynthesis remains uncertain. Taken together, our results revealed a previously unrecognized model of AaStuA in ACT biosynthesis that is critical for pathogenicity of A. alternata.