STEM CELL GENETICS LAB

Over prolonged culture, hPSCs are prone to acquiring recurrent genetic changes. Classically these have been observed as gross karyotypic abnormalities(Baker et al., 2007; Draper et al., 2004). More recently however, gains of point mutations in common oncogenes have been reported at a comparable rate (Avior, Eggan, & Benvenisty, 2019; Merkle et al., 2017). These changes pose concerns for the safe therapeutic use of hPSCS in regenerative medicine.  For these variants to rise to prevalence in culture, mutation must occur, the basis of which is genome damage. 

My research aims to explore the unique characteristics of hPSC metabolism and cell cycle as well as the conditions under which they are cultured to try to elucidate the specific molecular mechanisms underlying their genome damage. A better understanding of the genomic insults faced by hPSCs will inform improved culture conditions to ameliorate the perceived genomic instability of these cells.

I joined the Barbaric lab as postdoctoral researcher in March 2023. I completed my PhD at King's College London focusing on characterising hiPSC spheroids using high content analysis with an interest to dissect the effects of biochemical cues and physical
confinement on a 3D hiPSC.

Previous research in the Barbaric group revealed that hPSC variant cells have a selective growth advantage over wild-type cells when cell competition occurs during co-culture. The variants' overtake of culture arises through competitive interactions in cell-ECM adhesion and cell-cell adhesion.

My current research is to investigate the role of mechanosensing at cell-ECM adhesions in hPSC variant versus wild-type. I aim to reveal the optimal culture environment for wild-type hPSCs to minimise hPSC variant selective advantage during culture.

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Charcot-Marie-Tooth disease is the most common form of inherited peripheral neuropathy and is categorised into many types; Type 2A has a more severe clinical phenotype with no effective therapeutics for patients.

My PhD focuses on modelling Charcot-Marie-Tooth disease Type 2A (CMT2A) using hESCs to try and uncover new disease mechanisms that further our understanding of the disease, which could potentially lead to new therapeutics.

I use CRISPR editing, neuronal differentiations, and a host of live imaging and molecular biology approaches to study the consequences of disease-causing mutations in a disease-relevant cell type of human origin.

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