My research program is aimed at understanding how and why pancreatic Beta cells are destroyed in Type 1 Diabetes.

My projects involve using mouse models of Type 1 and Type 2 diabetes to investigate molecular pathways that can be targeted for developing novel therapies

I am trained as a molecular geneticist, with expertise in epigenetics, chromatin biology and stem cell biology.For my PhD work, I studied the function of a class of histone lysine methyltransferases (KMTs) that modify Histone H3K9, specifically in the context of embryonic stem cells. H3K9 di- and trimethylation by the KMTs SETDB1, G9a and GLP leads to gene silencing and disruption of H3K9 methylation pathways causes congenital anomaly disorders associated with intellectual disability (e.g. Kleefstra syndrome OMIM:610253) and their over-expression is frequently associated with malignant tumour growth in humans. My work uncovered a novel mechanism of action for these KMTs through a protein called hnRNP K, which to help them get to their target genes. Recent work on hnRNP K indicates that it too is essential for human development, with loss of function variants in this gene leading to Au-Kline syndrome (OMIM:616580). My work therefore has important implications for understanding the etiology of genetic disorders resulting from disruption of H3K9 methylation pathways and cancers where H3K9 KMTs are over-expresed.

My MSc thesis project involved mouse handling and genetic analysis, protein biochemistry including antibody testing and validation, gel filtration chromatography and immunoprecipitation.