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Candida albicans is the most common fungal pathogen of humans. Frequently found within the digestive tracts of healthy individuals, C. albicans is an opportunistic pathogen that can cause a wide variety of clinical syndromes in individuals with compromised immune systems. C. albicans has the remarkable ability to adapt to and invade virtually every human tissue; little is known, however, about how these adaptations are achieved.
In Saccharomyces cerevisiae --the most commonly studied species of yeast, and a close relative of C. albicans --global regulation of pre-mRNA splicing mediates specific responses to various environmental stresses. This raises the provocative idea that eukaryotic pathogens like C. albicans may have co-opted this form of gene regulation for survival within hostile host environments.
I have designed specialized microarrays to measure the splicing efficiency of every intron-containing C. albicans transcript. I am currently using these microarrays to study the response both to external environmental cues and to different developmental programs important for host invasion. I am also using a genetic approach to identify splicing factors that mediate these responses. Ultimately, we hope to identify novel drug targets for the treatment of C. albicans infections.
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