Prize Fellow
4 South 1.49
Email: s.diezmann@bath.ac.uk
Tel: +44 (0) 1225 383128
Twitter: @DiezmannLab
Academic Biography
2009 – 2013
- Postdoctoral Fellow, University of Toronto, Ontario, Canada
2002 – 2009
- Ph.D., Duke University, Durham, North Carolina, USA
1997 – 2002
- Biology Diploma, Humboldt University, Berlin, Germany
Dr Stephanie Diezmann
Profile
Research Interests
Every year 700 people die in the UK of a disease called candidemia. This infection is caused by a fungus, Candida albicans. Candidemia affects the weakest of the weak, such as low-birth weight infants and cancer chemotherapy patients. Unlike many other infectious microbes, C. albicans is not acquired from the environment but lives in most people’s mouths and intestines without causing any problems while they are healthy. Upon changes in immune status, however, C. albicans can turn into a deadly pathogen with mortality rates approaching 50%.
Infections with C. albicans are difficult to treat due to its close association with humans and the lack of appropriate fungal drug targets. Drug resistance in C. albicans is promoted by the molecular chaperone Hsp90. This heat shock proteins binds other proteins and keeps them poised for activation and in doing so interacts with up to 10% of the cell’s proteome. We mapped the Hsp90 genetic interaction network in Candida albicans showing that it is environmentally dependent and that it has changed substantially since C. albicans split from its close relative Saccharomyces cerevisiae several hundred million years ago (Diezmann et al., 2012).
We employ genomic and proteomic tools as well as standard yeast molecular biological techniques to understand how Hsp90 affects fungal virulence through its interaction network and through specific kinase interactors. Specifically, we are interested in understanding:
- How does the Hsp90 chaperone network change over evolutionary time and what are the consequences for environmental adaptation?
- How does kinase-mediated regulation of the Hsp90 complex affect fungal stress response pathways and virulence?
Publications
Singh-Babak, S.D., Babak, T., Diezmann, S., Hill, J. A., Xie, J. L., Chen, Y.-L., Poutanen, S. M., Rennie, R. P., Heitman, J. and Cowen, L. E., 2012. Global analysis of the evolution and mechanism of echinocandin resistance in Candida glabrata. PLoS Pathogens, 8 (5), e1002718.
Diezmann, S., Michaut, M., Shapiro, R. S., Bader, G. D. and Cowen, L. E., 2012. Mapping the Hsp90 genetic interaction network in Candida albicans reveals environmental contingency and rewired circuitry. Plos Genetics, 8 (3), e1002562.
Diezmann, S. and Dietrich, F.S., 2011. Oxidative stress survival in a clinical Saccharomyces cerevisiae isolate is influenced by a major quantitative trait nucleotide. Genetics, 188 (3), pp. 709-722.
Diezmann, S. and Dietrich, F.S., 2009. Saccharomyces cerevisiae: population divergence and resistance to oxidative stress in clinical, domesticated and wild isolates. PLoS ONE, 4 (4), e5317.
Al-Jawabreh, A., Diezmann, S., Müller, M., Wirth, T., Schnur, L.F., Strelkova, M.V., Kovalenko, D.A., Razakov, S.A., Schwenkenbecher, J., Kuhls, K. and Schönian, G., 2008. Identification of geographically distributed sub-populations of Leishmania (Leishmania) major by microsatellite analysis. BMC Evolutionary Biology, 8, 183.
View more publications »
