Abstract:
Candida albicans is the most prevalent human fungal pathogen. Unfortunately, there still
remains much that is unknown about it, including the reason for maintaining a diploid genome
and the function of many genes. In this thesis I describe the phenotypic consequences of up and
downregulating Pseudouridine Synthase 4 (PUS4) of C. albicans, as well as an examination of
the differences in the expression level of the entire transcriptome. These experiments and
resulting bioinformatic analysis have lead to our conclusion that that PUS4A is more lowly
transcribed than PUS4B. This data suggests PUS4A may be nonfunctional or play a different role
in C. albicans biology.