ROLE AND REGULATION OF CLN3 IN CANDIDA ALBICANS

Abstract

Candida albicans is a commensal fungus and an opportunistic pathogen. In immunocompromised and immunosuppressed individuals, C. albicans can cause serious bloodstream infections associated with high mortality rates. The ability to switch between yeast and hyphal morphologies is an important virulence factor of C. albicans. In response to numerous environmental signals, hyphal signaling pathways are activated resulting in filamentous growth. Interestingly, cell cycle arrest can also trigger filament formation; however the pathways involved are not well-understood. The work in this thesis demonstrates that the cAMP-PKA pathway is involved in filamentous growth during G1 arrest by Cln3-depletion and that S phase arrest by hydroxyurea treatment causes filamentation via a distinct mechanism. The role of Cln3 in C. albicans hyphal growth was also explored, with results suggesting that Cln3 may play an inhibitory role in hyphal growth. Lastly, the regulation of Cln3 by cyclin dependent kinases was briefly investigated.