PhD Research Project

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Mechanisms of asymmetric stem cell division

Institution:

University of Dundee

Dept/School/Faculty:

College of Life Sciences

PhD Supervisor:

Dr J Januschke

Application Deadline:

Applications accepted all year round

Funding Availability:

Funded PhD Project (Students Worldwide)

PhD Research Project

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Despite tremendous progress, the cells-of-origin of many cancers remain unknown. This strikingly applies to tissues of epithelial origin that are remarkably frequent to develop tumours. An important feature of epithelia is that they are maintained by the action of stem cells. Stem cells can generate different cell types in a single division, a process called asymmetric cell division. This is a key mechanism to establish different cell fates when building the tissue during development and also to maintain it during adulthood. One intriguing possibility is that errors in stem cell division might unchain the proliferative potential of stem cells and cause daughter cells to proliferate out of control. We aim to investigate the mechanisms behind asymmetric stem cell division to understand the link between stem cells and tumourigenesis.

Work in Drosophila neural stem cells has shown that impairing asymmetric cell division of stem cells can indeed trigger tumour growth. Stem cells in Drosophila can be unambiguously identified, genetically manipulated and followed by life cell imaging over consecutive rounds of cell division offering a unique advantage over other stem cell models.

The project aims to probe into the mechanism used by neural stem cells of the developing central nervous system to generate different cell fates. This involves the analysis of the dynamics of cell polarisation using advanced VIDEO microscopy as well as super resolution microscopy, genetics and molecular biology techniques such as recombineering.
A background in cell or developmental biology is desirable as well as a strong interest in microscopy. Previous experience with Drosophila is advantageous but not a requirement.