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The pathogenic fungus  Cryptococcus neoformans  uses the Bwc1-Bwc2 photoreceptor complex to regulate mating in response to light, virulence and ultraviolet radiation tolerance. How the complex controls these functions is unclear. Here, we identify and characterize a gene in  Cryptococcus ,  UVE1 , whose mutation leads to a UV hypersensitive phenotype. The homologous gene in fission yeast  Schizosaccharomyces pombe  encodes an apurinic/apyrimidinic endonuclease acting in the UVDE-dependent excision repair (UVER) pathway.  C. neoformans UVE1  complements a  S. pombe uvde  knockout strain.  UVE1  is photoregulated in a Bwc1-dependent manner in  Cryptococcus , and in  Neurospora crassa  and  Phycomyces blakesleeanus  that are species that represent two other major lineages in the fungi. Overexpression of  UVE1  in  bwc1  mutants rescues their UV sensitivity phenotype and gel mobility shift experiments show binding of Bwc2 to the  UVE1  promoter, indicating that  UVE1  is a direct downstream target for the Bwc1-Bwc2 complex. Uve1-GFP fusions localize to the mitochondria. Repair of UV-induced damage to the mitochondria is delayed in the  uve1  mutant strain. Thus, in  C. neoformans UVE1  is a key gene regulated in response to light that is responsible for tolerance to UV stress for protection of the mitochondrial genome.

The Uve1 Endonuclease Is Regulated by the White Collar Complex to Protect Cryptococcus neoformans from UV Damage