PhD Students

 

PhD Students have to register through the Crick Institute programme

Alex Hunt: How is the motility apparatus of Toxoplasma gondii and Plasmodium falciparum regulated in time and space.

 

This is a joint project with Jake Baum from Imperial College London and looks at the regulators of motility in Toxoplasma gondii and Plasmodium falciparum. The venture point for this project is the previous identification of a subset of proteins identified to be differentially phosphorylated in Toxoplasma CDPK3 mutant parasite lines and I predict that these are direct regulators of motility. Ongoing work in the Baum lab centres on the regulation of Plasmodium falciparum motility and invasion of the host cell and I will make best use of the expertise and experimental models in both labs to answer the question how motility is regulated in apicomplexan parasites.

 

Hugo Belda: What is the function of post-translational modification in supporting P. falciparum’s whole-sale take over of a red blood cell?
 

P. falciparum exports a large number of proteins out into its host red blood cell. These proteins drive the transformation of red blood cells from oxygen-transporting cells with no nucleus and little of a typical cell’s internal machinery into a parasite-production facility that causes all of malaria’s most severe symptoms.  We and others have found that many of these exported proteins are phosphorylated, but the kinases responsible are not currently known and—most importantly—the functional consequences are a mystery. I am using quantitative phoshoproteomic methods and at the same time am developing new genetic tools to try and figure out how P. falciparum uses post-translational modification to take over red blood cells and cause disease. 

Simon Butterworth: How do Toxoplasma effector proteins influence different tell types?
 

Toxoplasma secretes a substantial number of effector proteins into its host cell. How these interact with different cell types, in different hosts is not very well understood. I make use of our targeted CRIPSR libraries to measure the impact of individual effector proteins on different cell types in vivo and in vitro on a single cell level.