3. Dissection of UME6 Truncation Mutants Effects on C. albicans Filamentous Growth

Olivia Smith Ball State University, Ben Evans Ball State University
Faculty Sponsor(s): Douglas Bernstein Ball State University
Candida albicans is a human fungal pathogen with the potential of causing a lethal infection known as Candidiasis in immunocompromised individuals. C. albicans’s growth in the host is usually contained by the body’s immune response, however if an individual has a weakened immune system the C. albicans growth will not be kept in check and invasive C. albicans infection can occur. Infection of the bloodstream allows C. albicans to spread into other parts of the body and even other tissues, causing a systemic infection. Filamentous and yeast form growth are required for systemic infection. Resistance to many antifungal drugs further complicates treatment. To understand new antifungal drug targets, we need to better understand C. albicans at the molecular level. UME6 is a transcriptional regulator of filamentous growth in C. albicans. CRISPR-mediated recombination and restriction enzyme screening were used to create and verify mutants to truncate UME6. Mortality tests in Galleria mellonella larva and filamentation assays were used to characterize the mutants. The Bernstein lab has made a UME6 TAA truncation mutant to test the importance of the Zn2+ finger domain in the induction of filamentation. Mutants generated in the Bernstein lab have stop codons inserted prior to the DNA binding domain, also known as the Zn2+ finger domain. The truncation mutant in this experiment had decreased filamentation and virulence compared to the wild type but did not slow C. albicans growth. Work is ongoing to truncate UME6 downstream of the Zn2+ finger domain.
Biochemistry & Molecular Biology
Poster Presentation

When & Where

Irwin Library Lower Level