Dr Stephanie Diezmann


Each year, more people die of fungal infections than of malaria or tuberculosis worldwide. Our lab is interested in understanding how fungi cause disease in humans and aims to identify suitable targets to stop them. We investigate fungal pathogenicity by combining genetics, evolutionary theory, and molecular biology.


Our aim is to minimize the detrimental impact fungi have on human health and wellbeing. To do so, the lab is combining research into the cellular functions of the molecular chaperone Hsp90 with a targeted analysis of specific Hsp90 clients and their role in fungal virulence.

Our long-term goals include (i) the development of a novel drug target to be used in combination therapy with existing Hsp90 inhibitors, (ii) a detailed understanding of the evolution of Hsp90 genetic interaction networks, and (iii) the advancement of a new invertebrate host model to reduce numbers of commonly used vertebrate models.


We aim to understand how fungi cause disease in humans and identify novel drug targets in the fungal cell to develop more effective antifungal therapies.


The lab uses genetics and molecular biology to understand Hsp90’s role in fungal virulence with the long-term goal of identifying novel drug targets. Hsp90 is a molecular chaperone that stabilizes numerous signal transducers inside the cell and plays a central role in regulating fungal virulence. We previously showed that Hsp90 interacts with ~5% of the Candida albicans genome with many of its interactors being relevant in the expression of virulence traits. Since Hsp90 is highly conserved and thus difficult to target exclusively, its clients may provide more suitable drug targets. We focus on the leading fungal pathogen of humans Candida albicans, which causes a diverse array of disease ranging from oral thrush to life-threatening systemic infections, which affect 400,000 people world-wide annually.

Currently our team is:

1)    Characterising how Hsp90’s interactions with specific kinases affect fungal virulence. Using molecular and biochemical approaches, we investigate Hsp90-kinase interactions, including those that regulate Hsp90 and those that are dependent on Hsp90.

2)    Mapping the evolutionary trajectories of Hsp90 genetic interaction networks. We are conducting chemical-genomic screens in fungal species covering ~300 million years of evolution to elucidate how these circuitries evolved.

3)    Developing caterpillars of the Tobacco Hornworm as a novel invertebrate model host. To test the virulence potential of specific genes, mutants are often passaged through mice, which is ethically questionable and expensive. To mitigate this, we aim to develop a novel invertebrate model by making use of the UK’s only Hornworm colony based at the University of Bath.

Qualifications and History for Dr Stephanie Diezmann

  • 2009: PhD, University Program in Genetics and Genomics, Duke University, USA
  • 2009 – 2013: Post-doctoral Fellow, Department of Molecular Genetics, University of Toronto, Canada
  • 2013 – 2015: Prize Fellow, University of Bath, UK
  • 2015 – 2018: Lecturer, University of Bath, UK
  • 2018 – present Senior Lecturer, University of Bristol, UK 


  • 2001: Undergraduate Research Fellowship, German Academic Exchange Service
  • 2002 – 2004: PhD Fellowship, Duke University Program in Genetics and Genomics
  • 2010 – 2012: Postdoctoral Fellowship, Ontario Ministry of Research and Innovation
  • 2012: International Society for Human and Animal Mycology Young Investigator Award in Clinical Mycology

Selected Publications

  • Diezmann S, MD Leach, LE Cowen. 2015. Functional divergence of Hsp90 genetic interactions in biofilm and planktonic cellular states. PLoS ONE. 10(9): e0137947-20
  • Diezmann S. 2014. Oxidative stress response and adaptation to H2O2 in the model eukaryote Saccharomyces cerevisiae and its human pathogenic relatives Candida albicans and Candida glabrata. Fungal Biology Reviews 28: 126
  • Diezmann S, M Michaut, RS Shapiro, GD Bader, LE Cowen. 2012. Mapping the Hsp90 genetic interaction network in Candida albicans reveals environmental contingency and rewired circuitry. PLoS Genetics 8(3): e10002562
  • Diezmann S, FS Dietrich. 2011. Oxidative stress survival in a clinical Saccharomyces cerevisiae isolate is influenced by a major quantitative trait nucleotide. Genetics 188(3): 709
  • Diezmann S, CJ Cox, G Schönian, RJ Vilgalys, TG Mitchell. 2004. Phylogeny and evolution of medical species of Candida and related taxa: a multigenic analysis. Journal of Clinical Microbiology. 42(12): 5624


Our lab is/was generously funded by the MRC, BBSRC, Royal Society, and the ERC’s Marie Curie Initiative.


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