Characterization of the Aspergillus flavus rdiA gene with a rdi1∆ mutant of C. neoformans

Characterization of the Aspergillus flavus rdiA gene with a rdi1∆ mutant of C. neoformans

Oral - Basic

Several members in the Aspergillus genus produce aflatoxin, the most potent naturally occurring carcinogen known. Regulation of aflatoxin biosynthesis has been studied for several decades as this mycotoxin is currently regulated by the USDA. While all the biosynthetic steps have been characterized, much remains to be elucidated regarding the regulatory network controlling its production. Expression data show that A. flavus rdiA clusters with the aflatoxin pathway-specific transcriptional regulator aflR. Deletion of rdiA resulted in increased septation interval and branching as well as severely decreased AF production. The ∆rdiA mutant phenotype is similar to the rdi1∆ mutant of C. neoformans and the bem4∆ mutant in S. cerevisiae that exhibits a severe growth defect on minimal medium, a moderate growth defect on complete medium, and a cold temperature sensitivity phenotype. Interestingly, A. flavus rdiA expression at least partially rescues the cold-sensitive phenotype of the S. cerevisiae bem4∆ mutant. Additionally, it has been demonstrated that in contrast to S. cerevisiae, the mutant of C. neoformans RDI1 exhibits discernable morphological phenotypes, similar to the rdiA mutant of A. flavus. Therefore, we will complement the rdiA mutant of A. flavus to confirm the observed phenotypes in A flavus. Furthermore, we will complement the C. neoformans rdi1∆ mutant with A. flavus rdiA to establish the identity of the A flavus rdiA gene.