Differentially expressed genes of cir1 mutants in low iron or high iron medium

Iron overload is known to exacerbate many infectious diseases and, conversely, iron withholding is an important defense strategy for mammalian hosts. The mechanisms by which fungal pathogens sense iron in the mammalian host environment are poorly understood. The AIDS-associated pathogen Cryptococcus neoformans provides a unique opportunity to explore iron sensing in the context of infection because iron levels control elaboration of the polysaccharide capsule that is the major virulence factor of the fungus. Additionally, excess iron exacerbates experimental cryptococcosis. We identified the iron-responsive transcription factor Cir1 that regulates iron acquisition in C. neoformans and discovered that Cir1 also controls the expression of all of the known major virulence factors of the fungus. In particular, cir1 mutants are defective in capsule formation and avirulent in a mouse model of cryptococcosis. Thus the ability to sense iron is critical during infection by C. neoformans and may represent a target for antifungal therapy. Keywords: wt/mutant x low/high iron The following loop design, which includes three biological replicates and consists of four nodes and paths including dye-swap, was adopted for this study: wild-type (low iron) vs wild-type (high iron), wild-type (low iron) vs cir1delta (low iron), wild-type (high iron) vs cir1delta (high iron), and cir1delta (low iron) vs cir1delta (high iron). A total of 24 arrays were used for the experiment.