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Evolution of pathogenicity and sexual reproduction in eight Candida genomes

Author

Listed:
  • Geraldine Butler

    (UCD School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland)

  • Matthew D. Rasmussen

    (Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, Massachusetts 02139, USA)

  • Michael F. Lin

    (Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, Massachusetts 02139, USA
    Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

  • Manuel A. S. Santos

    (University of Aveiro)

  • Sharadha Sakthikumar

    (Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

  • Carol A. Munro

    (School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK)

  • Esther Rheinbay

    (Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, Massachusetts 02139, USA
    Bioinformatics Program, Boston University, Boston, Massachusetts 02215, USA)

  • Manfred Grabherr

    (Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

  • Anja Forche

    (Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 55455, USA)

  • Jennifer L. Reedy

    (Duke University Medical Center, Durham, North Carolina 27710, USA)

  • Ino Agrafioti

    (Centre for Bioinformatics, Imperial College London, Wolfson Building, South Kensington, London SW7 2AY, UK)

  • Martha B. Arnaud

    (Stanford University Medical School Stanford)

  • Steven Bates

    (School of Biosciences, University of Exeter)

  • Alistair J. P. Brown

    (School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK)

  • Sascha Brunke

    (Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute)

  • Maria C. Costanzo

    (Stanford University Medical School Stanford)

  • David A. Fitzpatrick

    (UCD School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland)

  • Piet W. J. de Groot

    (Swammerdam Institute for Life Sciences, University of Amsterdam)

  • David Harris

    (Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus)

  • Lois L. Hoyer

    (University of Illinois at Urbana-Champaign, Urbana, Illinois 61802, USA)

  • Bernhard Hube

    (Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute)

  • Frans M. Klis

    (Swammerdam Institute for Life Sciences, University of Amsterdam)

  • Chinnappa Kodira

    (Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA
    Present address: 454 Life Sciences, 20 Commercial Street, Branford, Connecticut 06405, USA.)

  • Nicola Lennard

    (Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus)

  • Mary E. Logue

    (UCD School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland)

  • Ronny Martin

    (Leibniz Institute for Natural Product Research and Infection Biology - Hans Knöll Institute)

  • Aaron M. Neiman

    (SUNY Stony Brook, Stony Brook, New York 11794, USA)

  • Elissavet Nikolaou

    (School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK)

  • Michael A. Quail

    (Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus)

  • Janet Quinn

    (Institute for Cell and Molecular Biosciences, Newcastle University)

  • Maria C. Santos

    (University of Aveiro)

  • Florian F. Schmitzberger

    (Stanford University Medical School Stanford)

  • Gavin Sherlock

    (Stanford University Medical School Stanford)

  • Prachi Shah

    (Stanford University Medical School Stanford)

  • Kevin A. T. Silverstein

    (Biostatistics and Bioinformatics Group, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota 55455, USA)

  • Marek S. Skrzypek

    (Stanford University Medical School Stanford)

  • David Soll

    (The University of Iowa, Iowa City, Iowa 52242, USA)

  • Rodney Staggs

    (Biostatistics and Bioinformatics Group, Masonic Cancer Center, University of Minnesota, Minneapolis, Minnesota 55455, USA)

  • Ian Stansfield

    (School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK)

  • Michael P. H. Stumpf

    (Centre for Bioinformatics, Imperial College London, Wolfson Building, South Kensington, London SW7 2AY, UK)

  • Peter E. Sudbery

    (University of Sheffield)

  • Thyagarajan Srikantha

    (The University of Iowa, Iowa City, Iowa 52242, USA)

  • Qiandong Zeng

    (Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

  • Judith Berman

    (Cell Biology and Development, University of Minnesota, Minneapolis, Minnesota 55455, USA)

  • Matthew Berriman

    (Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus)

  • Joseph Heitman

    (Duke University Medical Center, Durham, North Carolina 27710, USA)

  • Neil A. R. Gow

    (School of Medical Sciences, Institute of Medical Sciences, University of Aberdeen, Foresterhill, Aberdeen AB25 2ZD, UK)

  • Michael C. Lorenz

    (The University of Texas Health Science Center at Houston, Houston, Texas 77030, USA)

  • Bruce W. Birren

    (Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

  • Manolis Kellis

    (Computer Science and Artificial Intelligence Laboratory, MIT, Cambridge, Massachusetts 02139, USA
    Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

  • Christina A. Cuomo

    (Broad Institute of MIT and Harvard, Cambridge, Massachusetts 02142, USA)

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/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.

Suggested Citation

  • Geraldine Butler & Matthew D. Rasmussen & Michael F. Lin & Manuel A. S. Santos & Sharadha Sakthikumar & Carol A. Munro & Esther Rheinbay & Manfred Grabherr & Anja Forche & Jennifer L. Reedy & Ino Agra, 2009. "Evolution of pathogenicity and sexual reproduction in eight Candida genomes," Nature, Nature, vol. 459(7247), pages 657-662, June.
    • Handle: RePEc:nat:nature:v:459:y:2009:i:7247:d:10.1038_nature08064
    DOI: 10.1038/nature08064
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