Defining the role of phosphate acquisition in promoting stress resistance and virulence in a major fungal pathogen of humans (Newcastle)
Candida albicans is the major fungal pathogen of humans causing over 400,000 deaths per annum. Systemic Candida infections are difficult to treat as current anti-fungal drugs are limited and cause undesirable side-effects. It is of vital importance to understand how C. albicans mounts responses to stresses encountered within the human host, because such responses are essential for the virulence of this major pathogen. In this project you will explore exciting new findings from the Quinn lab that phosphate metabolism is vital for C. albicans stress resistance and virulence by regulating metal homeostasis. You will receive training in three vibrant laboratories in diverse areas including molecular genomics, mass spectrometry, cellular stress responses, biology of metals, and virulence models, to explore the mechanisms by which phosphate acquisition mediates fungal virulence. This will be an important step in the development of improved therapeutic strategies for treating life-threatening fungal infections.
For further information see the website: http://www.ncl.ac.uk/camb/
Please submit a full CV and covering letter directly to [email protected]
This is a 4 year BBSRC studentship under the Newcastle-Liverpool-Durham DTP. The successful applicant will receive research costs, tuition fees and stipend (£14,057 for 2015-16). The PhD will start in September 2016. Applicants should have, or be expecting to receive, a 2.1 Hons degree (or equivalent) in a relevant subject. EU candidates must have been resident in the UK for 3 years in order to receive full support. There are 2 stages to the application process.
Patterson MJ, McKenzie CG, Smith DA, da Silva Dantas A, Sherston S, Veal EA, Morgan BA, MacCallum DM, Erwig LP, Quinn J. (2013) Ybp1 and Gpx3 signaling in Candida albicans govern hydrogen peroxide-induced oxidation of the Cap1 transcription factor and macrophage escape. Antioxid Redox Signal. 19(18):2244-60.