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Eukaryotic Cell, June 2007, p. 907-918, Vol. 6, No. 6
1535-9778/07/$08.00+0 doi:10.1128/EC.00090-07
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Department of Molecular Microbiology and Immunology, Brown University, Providence, Rhode Island 02912,1 Genetics Group, Biotechnology Research Group, National Research Council of Canada, 6100 Royalmount Ave., Montreal, Quebec H4P 2R2, Canada2
Received 20 March 2007/ Accepted 30 March 2007
Mating in Candida albicans and Saccharomyces cerevisiae is regulated by the secretion of peptide pheromones that initiate the mating process. An important regulator of pheromone activity in S. cerevisiae is barrier activity, involving an extracellular aspartyl protease encoded by the BAR1 gene that degrades the alpha pheromone. We have characterized an equivalent barrier activity in C. albicans and demonstrate that the loss of C. albicans BAR1 activity results in opaque a cells exhibiting hypersensitivity to alpha pheromone. Hypersensitivity to pheromone is clearly seen in halo assays; in response to alpha pheromone, a lawn of C. albicans
bar1 mutant cells produces a marked zone in which cell growth is inhibited, whereas wild-type strains fail to show halo formation. C. albicans mutants lacking BAR1 also exhibit a striking mating defect in a cells, but not in
cells, due to overstimulation of the response to alpha pheromone. The block to mating occurs prior to cell fusion, as very few mating zygotes were observed in mixes of
bar1 a and
cells. Finally, in a barrier assay using a highly pheromone-sensitive strain, we were able to demonstrate that barrier activity in C. albicans is dependent on Bar1p. These studies reveal that a barrier activity to alpha pheromone exists in C. albicans and that the activity is analogous to that caused by Bar1p in S. cerevisiae.
Published ahead of print on 6 April 2007.
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