Butler, Geraldine and Rasmussen, Matthew D. and Lin, Michael F. and Santos, Manuel A. and Sakthikumar, Sharadha and Munro, Carol A. and Rheinbay, Esther and Grabherr, Manfred and Forche, Anja and Reedy, Jennifer L. and Agrafioti, Ino and Arnaud, Martha B. and Bates, Steven and Brown, Alistair J.P. and Brunke, Sascha and Costanzo, Maria C. and Fitzpatrick, David A. and de Groot, Piet W. J. and Harris, David and Hoyer, Lois L. and Hube, Bernhard and Klis, Frans M. and Kodira, Chinnappa and Lennard, Nicola and Logue, Mary E. and Martin, Ronny and Neiman, Aaron M. and Nikolaou, Elissavet and Quail, Michael A. and Quinn, Janet and Santos, Maria C. and Schmitzberger, Florian F. and Sherlock, Gavin and Shah, Prachi and Silverstein, Kevin A.T. and Skrzypek, Marek S. and Soll, David and Staggs, Rodney and Stansfield, Ian and Stumpf, Michael P.H. and Sudbery, Peter E. and Srikantha, Thyagarajan and Zeng, Qiandong and Berman, Judith and Berriman, Matthew and Heitman, Joseph and Gow, Neil A.R. and Lorenz, Michael C. and Birren, Bruce W. and Kellis, Manolis and Cuomo, Christina A.
(2009)
Evolution of pathogenicity and sexual reproduction in eight Candida genomes.
Nature, 459.
pp. 657-662.
ISSN 1476-4687
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.
Item Type: |
Article
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Additional Information: |
This article is distributed under the terms of the Creative Commons Attribution-Non-Commercial-Share Alike licence (http://creativecommons.org/licenses/by-nc-sa/3.0/), which permits distribution, and reproduction in any medium, provided the original author and source are credited. This license does not permit commercial exploitation, and derivative works must be licensed under the same or similar licence. |
Keywords: |
Evolution of pathogenicity; sexual reproduction; Candida genomes; |
Academic Unit: |
Faculty of Science and Engineering > Biology |
Item ID: |
11065 |
Identification Number: |
https://doi.org/10.1038/nature08064 |
Depositing User: |
David Fitzpatrick
|
Date Deposited: |
19 Sep 2019 16:41 |
Journal or Publication Title: |
Nature |
Publisher: |
Nature Publishing Group |
Refereed: |
Yes |
URI: |
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Use Licence: |
This item is available under a Creative Commons Attribution Non Commercial Share Alike Licence (CC BY-NC-SA). Details of this licence are available
here |
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