1. UCD School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland
2. Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, Massachusetts 02139, USA
3. Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA
4. Department of Biology and CESAM, University of Aveiro, 3810-193 Aveiro, Portugal
5. School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK
6. Bioinformatics Program, Boston University, Boston, Massachusetts 02215, USA
7. Department of Genetics, Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 55455, USA
8. Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA
9. Centre for Bioinformatics, Imperial College London, Wolfson Building, South Kensington, London SW7 2AY, UK
10. Department of Genetics, Stanford University Medical School Stanford, California 94305-5120, USA
11. School of Biosciences, University of Exeter, Exeter EX4 4QD, UK
12. Department of Microbial Pathogenicity Mechanisms, Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute, D-07745 Jena, Germany
13. Swammerdam Institute for Life Sciences, University of Amsterdam, 1090 GB Amsterdam, The Netherlands
14. Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton CB10 1SA, UK
15. Department of Pathobiology, University of Illinois at Urbana-Champaign, Urbana, Illinois 61802, USA
16. Department of Biochemistry and Cell Biology, SUNY Stony Brook, Stony Brook, New York 11794, USA
17. Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne NE2 4HH, UK
18. Biostatistics and Bioinformatics Group, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota 55455, USA
19. Department of Biology, The University of Iowa, Iowa City, Iowa 52242, USA
20. Department of Molecular Biology and Biotechnology, University of Sheffield, Sheffield S10 2TN, UK
21. Department of Microbiology and Molecular Genetics, The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA
22. Present address: 454 Life Sciences, 20 Commercial Street, Branford, Connecticut 06405, USA.
23. These authors contributed equally to this work.

Correspondence to: Geraldine Butler¹Manolis Kellis^2,3,23Christina A. Cuomo^3,23 Correspondence and requests for materials should be addressed to C.A.C. (Email: cuomo@broad.mit.edu), M.K. (Email: manoli@mit.edu) or G.B. (Email: geraldine.butler@ucd.ie).

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Abstract

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 a1/2 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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