Molecular characterisation of fungal environmental carbon dioxide sensing and its integration with cAMP signalling and metabolism.

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The fungal pathogen Candida albicans is non-virulent in healthy individuals where it is part of the normal skin and intestinal flora. On the contrary, in patients whose immune system is not functional as a consequence of cancer, age, or AIDS, this fungus is a major cause of death. C. albicans undergoes a series of characteristic morphological changes important for its ability to cause damage to the infected host. These changes are controlled by host environmental cues such as the elevated temperature inside the body, the slightly alkaline pH of blood as well as high carbon dioxide concentrations. Inside our body the concentration of carbon dioxide is approximately 150 fold higher than in the air surrounding us. When the fungal pathogen C. albicans senses the higher CO2 inside the host, it initiates a series of morphological changes, which enable it to infect that host. Recently we identified the enzyme from C. albicans responsible for these changes. Now we want to investigate precisely how this enzyme senses CO2. CO2 serves other functions important for the survival of C. albicans. For example it is a fundamental part of basic cellular metabolism. We also propose to study whether the CO2 sensing enzyme is related to C. albicans metabolism. Interfering with fungal CO2 sensing may open up possibilities to better manage C. albicans infection in the future.