Journal
NATURE
Volume 459, Issue 7247, Pages 657-662Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nature08064
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Funding
- US National Human Genome Research Institute (NHGRI)
- Fungal Genome Initiative at the Broad Institute
- Wellcome Trust
- NHGRI
- National Institute of Allergy and Infectious Disease
- US National Institutes of Health (NIH)
- Department of Health and Human Services
- Science Foundation Ireland
- NIH
- US National Science Foundation
- Sloan Foundation
- BBSRC [BB/F007892/1, BB/F00513X/1, BB/F013566/1] Funding Source: UKRI
- MRC [G0400284] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/F00513X/1, BB/F007892/1, BB/F013566/1] Funding Source: researchfish
- Medical Research Council [G0400284] Funding Source: researchfish
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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 alpha 1/alpha 2 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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