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Assistant Professor Mailing Address: Current Research Interests
A genetic model for Neurofibromatosis Type II: Identification and characterization of protein partners of the Merlin tumour suppressor protein
We study the molecular mechanisms that link polarity and proliferation in epithelial cells. When cells lose this linkage they often become metastatic. Specifically, we use Drosophila melanogaster (the fruit fly) as a genetic model to study Neurofibromatosis Type 2 (NF2), an inherited cancer of the brain and spinal cord. Mutation or loss of the NF2 gene is also associated with metastasis of several non-neuronal tumours. Merlin, the protein product of the NF2 gene, is a tumour suppressor that interacts with the plasma membrane and the cytoskeleton. However, the molecular mechanism of how Merlin acts as a tumour suppressor is not known. To address this question, we are taking the approach of identifying and characterizing proteins that interact with Merlin. Drosophila provides a unique toolbox of powerful genetic techniques to determine the function of Merlin and its interacting proteins. We have already identified several proteins that interact with Merlin, and are currently studying how these control proliferation and adhesion within the cell. We hypothesize that Merlin is functioning as part of a multi-protein complex to control proliferation and polarity. Other proteins include kinases, scaffold proteins and proteins involved in post-transcriptional regulation. The approaches we use include genetic analysis, molecular and cell biology, biochemistry, and advanced microscopy. Recent Publications Hughes, S.C. and R.G. Fehon. (2007). Understanding ERM Proteins – The awesome power of genetics finally brought to bear. Current Opinion in Cell Biology, 19:51-56. Hughes, S.C. and R.G. Fehon. (2006). Phosphorylation and activity of the tumor-suppressor Merlin and ERM protein Moesin are coordinately regulated by the Slik kinase. Journal of Cell Biology, 175(2):305-313.
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