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Inositol polyphosphate kinases and fungal virulence


Project Description

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 important to understand how C. albicans acquires essential nutrients during infection of the human host, because this is intimately linked with the virulence of this major pathogen. In this project you will explore exciting new findings from the Quinn lab that acquisition of the macronutrient phosphate is vital for C. albicans virulence. Specifically, building on a recent breakthrough in the field, you will determine how C. albicans senses intracellular levels of phosphate to trigger activation of the PHO phosphate acquisition pathway. Using a multidisciplinary approach, you will be trained in molecular genomics, biochemistry, and virulence models, to explore the role of inositol polyphosphate signalling molecules in mediating phosphate homeostasis and fungal virulence. This is an important step in the development of improved therapeutic strategies for treating fungal infections.

HOW TO APPLY

Applications should be made by emailing with a CV (including contact details of at least two academic (or other relevant) referees), and a covering letter – clearly stating your first choice project, and optionally 2nd and 3rd ranked projects, as well as including whatever additional information you feel is pertinent to your application; you may wish to indicate, for example, why you are particularly interested in the selected project(s) and at the selected University. Applications not meeting these criteria will be rejected.
In addition to the CV and covering letter, please email a completed copy of the Additional Details Form (Word document) to . A blank copy of this form can be found at: https://www.nld-dtp.org.uk/how-apply.
Informal enquiries may be made to .

Funding Notes

This is a 4 year BBSRC studentship under the Newcastle-Liverpool-Durham DTP. The successful applicant will receive research costs, tuition fees and stipend (£15,009 for 2019-20). The PhD will start in October 2020. 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. Please note, there are 2 stages to the application process.

References

The type VI secretion system deploys antifungal effectors against microbial competitors. Nat Microbiol. 2018, 3(8):920-931

Redox Regulation, Rather than Stress-Induced Phosphorylation, of a Hog1 Mitogen-Activated Protein Kinase Modulates Its Nitrosative-Stress-Specific Outputs. mBio 2018 9(2), e02229-17

Phosphate Acquisition and Virulence in Human Fungal Pathogens. Microorganisms 2017, 5(3), 48

Blocking two-component signalling enhances Candida albicans virulence and reveals adaptive mechanisms that counteract sustained SAPK activation. PLoS Pathogens 2017, 13(1), e1006131

Stress-induced nuclear accumulation is dispensable for Hog1-dependent gene expression and virulence in a fungal pathogen. Scientific Reports 2017, 7, 14340

Pho4 mediates phosphate acquisition in Candida albicans and is vital for stress resistance and metal homeostasis. Molecular Biology of the Cell 2016, 27(17), 2784-2801

Mechanisms underlying the delayed activation of the Cap1 transcription factor in Candida albicans following combinatorial oxidative and cationic stress important for phagocytic potency. mBio 2016, 7(2), e00331-16

Metabolomic profiling reveals a finely tuned, starvation-induced metabolic switch in Trypanosoma cruziepimastigotes. Journal of Biological Chemistry 2017 292(21): 8964-8977

Proline Metabolism is Essential for Trypanosoma brucei brucei Survival in the Tsetse Vector. PLoS Pathogens 2017, 13(1): e1006158

Role of Δ1-Pyrroline-5-Carboxylate Dehydrogenase Supports Mitochondrial Metabolism and Host-Cell Invasion of Trypanosoma cruzi. Journal of Biological Chemistry 2015, 290(12): 7767-7790

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