Candida species are the most common cause of opportunistic fungal infection worldwide. Here we report the genome sequences of six Candida species and compare these and related pathogens and non-pathogens. There are significant expansions of cell wall, secreted and transporter gene families in pathogenic species, suggesting adaptations associated with virulence. Large genomic tracts are homozygous in three diploid species, possibly resulting from recent recombination events. Surprisingly, key components of the mating and meiosis pathways are missing from several species. These include major differences at the mating-type loci (MTL); Lodderomyces elongisporus lacks MTL, and components of the a1/α2 cell identity determinant were lost in other species, raising questions about how mating and cell types are controlled. Analysis of the CUG leucine-to-serine genetic-code change reveals that 99% of ancestral CUG codons were erased and new ones arose elsewhere. Lastly, we revise the Candida albicans gene catalogue, identifying many new genes.
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Acknowledgements We thank the US National Human Genome Research Institute (NHGRI) for support under the Fungal Genome Initiative at the Broad Institute. We thank C. Kurtzman for providing the sequenced strains of L. elongisporus, C. guilliermondii and C. lusitaniae, M. Koehrsen for Broad Institute website support, D. Park for informatics support and K. Wolfe and A. Regev for comments on the manuscript. We acknowledge the contributions of the Broad Institute Sequencing Platform and A. Barron, L. Clark, C. Corton, D. Ormond, D. Saunders, K. Seeger and R. Squares from the Wellcome Trust Sanger Institute for the C. parapsilosis sequencing and assembly. N.A.R.G., A.J.P.B., M.B. and co-workers were supported by the Wellcome Trust; M.G., S.S., Q.Z., C.K., B.W.B. and C.A.C. were supported by NHGRI and the National Institute of Allergy and Infectious Disease, US National Institutes of Health (NIH), Department of Health and Human Services; G.B. and co-workers were supported by Science Foundation Ireland; J.B., A.F., J.H., A.M.N. and co-workers were supported by the NIH; and M.K., M.D.R. and M.F.L. by the NIH, the US National Science Foundation and the Sloan Foundation.