This Article Full Text (PDF) Other Versions of this Article: EC.00456-07v1 7/5/848    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Reprints and Permissions Copyright Information Books from ASM Press MicrobeWorld Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Muller, H. Articles by Fairhead, C. Search for Related Content PubMed PubMed Citation Articles by Muller, H. Articles by Fairhead, C.

 Previous Article  |  Next Article 

Eukaryotic Cell doi:10.1128/EC.00456-07
Copyright (c) 2008, American Society for Microbiology and/or the Listed Authors/Institutions. All Rights Reserved.

The asexual yeast Candida glabrata maintains distinct a and haploid mating types

Institut Pasteur, Unité de Génétique Moléculaire des Levures; CNRS URA 2171; Université Pierre et Marie Curie - Paris 6 UFR927; F75015 Paris, France; Université Pierre et Marie Curie - Paris 6; Faculté de Médecine St-Antoine; Parasitologie-Mycologie; F75012 Paris, France

^* To whom correspondence should be addressed. Email: hmuller{at}pasteur.fr.

	Abstract

The genome of the type strain of Candida glabrata (CBS138, ATCC2001) contains homologs of most of the genes involved in mating in S. cerevisiae, starting with the mating pheromone and receptor genes. Only haploid cells are ever isolated, but C. glabrata strains of both mating types are commonly found, the type strain being MAT, and most others, such as BG2, MATa. No sexual cycle has been documented in this species. In order to understand which steps of the mating pathway are defective, we have analysed the expression of homologs of some of the key genes involved, and also production of mating pheromones and sensitivity to artificial pheromones.We show that cells of opposite mating-types express both pheromone receptor genes, and are insensitive to pheromones. Nonetheless, cells maintain specificity through regulation of the 1 and 2 genes, and more surprisingly, through differential splicing the a1 transcript.