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Understanding signalling networks during malaria parasite infection and transmission

  • Full or part time
    Dr N Philip
  • Application Deadline
    Friday, March 01, 2019
  • Competition Funded PhD Project (European/UK Students Only)
    Competition Funded PhD Project (European/UK Students Only)

Project Description

Malaria threatens around 400 million people globally and results in over 0.5 million deaths annually, thereby continuing to be a major public health problem. Malaria is caused by the Plasmodium parasite, which completes its complex lifecycle in a mosquito vector and a mammalian host. While the asexual stage causes symptoms of disease in the host, sexual stage development is required for disease transmission. These two developmental stages of the parasite are regulated by numerous proteins whose actions are often controlled either by the addition (phosphorylation) or removal (dephosphorylation) of phosphate groups. Enzymes that catalyse the addition (kinases) and removal (phosphatases) of phosphate groups have long been considered valuable therapeutic targets in many human diseases such as cancer and diabetes, and more recently these enzymes have also been recognized as viable targets for anti-malarial therapy.
Protein phosphorylation is critical for the malaria parasite’s development and virulence (Philip et al, 2012; Philip and Haystead, 2007). However due to inadequate genetic tools, it was difficult to examine precise function of phosphorylation modulating enzymes essential for both asexual and sexual stages of the parasite. Recently we established a tool for conditional regulation of parasite protein levels that is inducible, rapid and specific (Philip and Waters, 2015). This tool revealed crucial roles for a parasite calcium-dependent protein phosphatase, Calcineurin, in regulating parasite colonisation of both the host and vector. In addition to Calcineurin, a third of the parasite’s kinome and phosphatome is expressed in both host and vector stages suggesting multifunctional roles during development and transmission. However roles of these critical enzymes and their associated regulators and substrates remain elusive.
We are seeking a passionate student to join our team where the focus of the project will be specifically tailored to the student’s interest. The PhD project will include innovative chemical-genetic and proteomic strategies to uncover signalling enzymes required for malaria parasite infection and transmission and, in turn discover identities of their substrates and regulators. Ultimately you will identify and characterise multifunctional enzymes, which could become robust infection and transmission blocking candidates. You will attend and present at weekly lab meetings, annual departmental meetings and additionally participate in national and international conferences.

https://www.ed.ac.uk/profile/dr-nisha-philip

Funding Notes

The “Apply online” button on this page will take you to our Online Application checklist. Please complete each step and download the checklist which will provide a list of funding options and guide you through the application process.

If you would like us to consider you for one of our scholarships you must apply by 12 noon on 1 March 2019 at the latest.

References

Nisha Philip and Waters AP. (2015). Conditional degradation of Plasmodium Calcineurin reveals functions in parasite colonization of both host and vector. Cell Host and Microbe, 18(1): 122-131
Nisha Philip, Vaikkinen HJ, Tetley L, Waters AP. (2012). A unique Kelch domain phosphatase in Plasmodium regulates ookinete morphology, motility and invasion. PLoS One, 9:e44617
Nisha Philip and Haystead TA. (2007) Characterization of a UBC13 kinase in Plasmodium falciparum. Proceedings of the National Academy of Sciences, USA. May 8;104(19):7845-50

How good is research at University of Edinburgh in Biological Sciences?

FTE Category A staff submitted: 109.70

Research output data provided by the Research Excellence Framework (REF)

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