Harriet Knafler

Investigating the role of endocytosis in the virulence of Candida albicans

I studied Microbiology at the University of Sheffield, and decided to stay in Sheffield to do my phD. I am working in Kathryn Ayscough’s lab, who study the process of endocytosis – the mechanism by which cells uptake substances from their environment. I am currently focusing on the endocytic adaptor complex AP2. I am investigating the role of AP2 in the virulence of Candida albicans. C.albicans is a fungal pathogen, which causes opportunistic infections which are particularly dangerous to immunocompromised patients. It is a common hospital-acquired pathogen, with a mortality rate of up to 40% for systemic infection. We hope to learn more about factors which are important to C.albicans virulence.

We have deleted an essential subunit of the AP2 endocytic adaptor complex in Candida albicans, and observed marked defects in polarised growth. As shown previously, the apm4 deletion mutant is unable to form long, thin filamentous cells under inducing conditions, instead growing wide and misshapen hyphae. The mutant is only slightly impaired in fluid phase endocytosis, leading us to hypothesise that AP2 plays a role in the endocytosis of specific cargoes which are important to polarised growth. It has recently become clear that a balance of endocytosis and secretion is essential for the highly polarised growth seen in filamentous fungi, however many of the key players remain unknown (Schultzhaus and Shaw, 2017). This polarised growth is a key aspect of cell biology, and is also central to Candida albicans virulence (Mayer et al., 2013). Therefore, elucidating the role of the AP2 endocytic adaptor complex in hyphal growth and virulence of Candida albicans is of great importance.