Evolution of pathogenicity and sexual reproduction in eight Candida genomes

UCD School of Biomolecular and Biomedical Science, Conway Institute, University College Dublin, Belfield, Dublin 4, Ireland.
Nature (Impact Factor: 41.46). 07/2009; 459(7247):657-62. DOI: 10.1038/nature08064
Source: PubMed


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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    • "Nonetheless, formation of allotriploids such as AWRI1499 and AWRI1608 most likely required some form of sexual cycle and there has been substantial loss-of-heterozygosity across the genomes of the two sequenced diploid strains, which in S. cerevisiae is associated with genome renewal through homothallism (Mortimer et al., 1994). Signatures of sex in genome assemblies are difficult to assess and predictions based solely upon presence or absence of key orthologs have proven inaccurate – for example, both sexual and asexual Candida species are missing some of the same notionally key genes involved in fungal meiosis (Butler et al., 2009), implying "
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