Proper coordination and control of cell division is critical to cells, and failure to properly manage the division process has severe consequences ranging from chromosomal aneuploidies to cell death. Thus, cell cycle regulation should be an attractive target for new antifungal development. However this process also represents a double-edged sword as many regulators will be evolutionarily conserved between the pathogenic yeast and its host.

Our hypothesis is that coupling bioinformatics in the post-genomic era with the understanding of the molecular events controlling key aspect of the Candida proliferation would, by facilitating the identification of exploitable biological targets and the subsequent development of new antifungal drugs, be an invaluable asset to efforts directed at the ultimately preventing, treating and controlling C. albicans infections.

We previously published the first genome-wide transcriptional analysis of the C. albicans cell cycle and compared it to those of Saccharomyces cerevisiae, S. pombe and humans (Côte et al., 2009, Mol. Biol. Cell). We found that many regulatory components found in humans and in the budding and fission yeasts are missing or used differently in C. albicans, suggesting that there are unique aspects of cell cycle regulation that can be identified in the pathogen. Such unique components of this essential process would provide promising targets for antifungal drug development.