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Candida glabrata (Torulopsis glabrata) is currently the second most frequent organism isolated from superficial and invasive fungal infections, after Candida albicans, and contrary to the latter, exhibits resistance to azole derivatives [1]. It is phylogenetically closer to Saccharomyces than to other Candida, despite its name. It is usually isolated from sites of infections or mammalian feces, but there is some evidence that it exists in other habitats [2]. It is a haploid yeast that can exhibit pseudohyphal growth [3]. Even though the genes homologous to mating and mating-type switching from S. cerevisiae are all found in the genome of C. glabrata [4, 5] and mating type switching has been reported [6, 7], no mating has ever been described and no diploid cells have been isolated.

Molecular genetic methods applied to this yeast include replicative and integrative transformation [8,9, 10], but the lack of a sexual cycle is a draw-back for classical genetics. A particular family of adhesins involved in pathogenicity, the subtelomeric EPA family, has been identified in this yeast [11].

The genome of strain CBS138 (type strain isolated from human feces) has been sequenced and reveals the presence of 13 chromosomes totalling 12.3Mb without the rDNA, which is organised into two distinct loci, on chromosomes 12 and 13. There are approx 5283 coding genes, and 207 tRNA genes. The strain contains two MAT-like loci with MATalpha information, and a third with MATa information. EPA genes in this strain are also part of a large subtelomeric family.

Compared to S. cerevisiae, with which it shares the common whole genome duplication in its ancestry, C. glabrata shows a significantly greater degree of gene loss, resulting in a regressive evolution (loss of specific functions).

1. Kaur R, Castano I, Cormack BP. 2004. Functional genomic analysis of fluconazole susceptibility in the pathogenic yeast Candida glabrata: roles of calcium signaling and mitochondria. Antimicrob Agents Chemother; 48(5):1600-13.
2. Kurtzman CP, Fell JW. 1997. In "The yeasts, a taxonomic study", Elsevier, Amsterdam.
3. Csank C, Haynes K. 2000. Candida glabrata displays pseudohyphal growth. FEMS Microbiol Lett;189(1):115-20.
4. Srikantha T, Lachke SA, Soll DR. 2003. Three mating type-like loci in Candida glabrata. Eukaryot Cell; 2(2):328-40.
5. Wong S, Fares MA, Zimmermann W, Butler G, Wolfe KH.2003. Evidence from comparative genomics for a complete sexual cycle in the 'asexual' pathogenic yeast Candida glabrata. Genome Biol; 4(2):R10.
6. Brockert PJ, Lachke SA, Srikantha T, Pujol C, Galask R, Soll DR. 2003. Phenotypic switching and mating type switching of Candida glabrata at sites of colonization. Infect Immun;71(12):7109-18.
7. Butler G, Kenny C, Fagan A, Kurischko C, Gaillardin C, Wolfe KH. 2004. Evolution of the MAT locus and its Ho endonuclease in yeast species. Proc Natl Acad Sci U S A;101(6):1632-7. Epub 2004 Jan 26.
8. Zhou P, Szczypka MS, Young R, Thiele DJ. 1994. A system for gene cloning and manipulation in the yeast Candida glabrata. Gene;142(1):135-40.
9. Kitada K, Yamaguchi E, Arisawa M. 1995. Cloning of the Candida glabrata TRP1 and HIS3 genes, and construction of their disruptant strains by sequential integrative transformation. Gene; 165(2):203-6.
10. Castano I, Kaur R, Pan S, Cregg R, Penas Ade L, Guo N, Biery MC, Craig NL, Cormack BP. 2003. Tn7-based genome-wide random insertional mutagenesis of Candida glabrata. Genome Res; 13(5):905-15.
11. Cormack BP, Ghori N, Falkow S. 1999. An adhesin of the yeast pathogen Candida glabrata mediating adherence to human epithelial cells. Science; 285(5427):578-82.