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Welcome to our lab website! Here you'll find information about who we are and what we do, as well as resources that we have for you to use.

Our lab is interested in how the malaria-causing parasite, Plasmodium falciparum, uses cytoskeletal filaments to organise its cellular components. We seek to understand the structure and function of these components using techniques such as single particle cryo-electron microscopy and single-molecule TIRF microscopy.

We are part of a vibrant research community in the Department of Biochemistry, University of Oxford in the Dorothy Crowfoot Hodgkin building. We are grateful to our funding from Wellcome.

We are committed to being open, collaborative and supportive both within our institute and within the wider research community. As such we are happy to share our expertise, data and resources. If you need anything, please reach out!

How does the malaria parasite cytoskeleton organise the cell?

In the human bloodstream, Plasmodium falciparum invades red blood cells to replicate inside, hidden away from the host immune system. To invade, the parasite uses specialised organelles, the rhoptries and micronemes. These organelles are held at the apical end of the cell, whereas its nucleus, mitochondria and other organelles are held toward the basal end. This striking polarised organisation is required for proper parasite function.

In higher eukaryotes, cell organisation is underpinned by its cytoskeleton, which forms an complex network that extends throughout the cell. In contrast the Plasmodium falciparum parasite maintains a much reduced cytoskeleton, which, though simplified, is still important for cell function. This is exemplified by the parasite's microtubules, cytoskeletal elements formed from the protein tubulin. In the blood-stage of the parasite life cycle, the parasite maintains two tubulin-based elements: centriolar plaques that are responsible for mitosis, and a small stable microtubule array that is rooted at the apex of the parasite, reaching back along the periphery of the cell towards the nucleus. Deleting tubulin results in parasites with aberrant organisation unable to invade host cells.

To interact with the rest of the cell microtubules recruit a myriad of microtubule-binding proteins, including molecular tethers and motors. However how these proteins function in parasites is not completely understood. We will dissect the function of proteins that bind to microtubules, as well as to other cytoskeletal elements, to see how they contribute to the organisation of the malaria parasite. Our research will contribute our understanding of how cytoskeletal proteins organise the eukaryotic cell, as well as identify targets future antimalarial therapeutic research.