Coordination of cellular programs – for example, the cell division cycle and cell metabolism – is essential for proper cellular homeostasis and cell physiology. Cells that exhibit failures in such coordination mechanism have high tendency towards acquisition of unstable genomes. Genomic instability is characterized by increased accumulation of point mutations, gene deletions, translocations, amplifications, loss or gain of whole chromosome(s) or chromosome part(s) (so called aneuploidy) and whole genome duplications (termed polyploidy). Genomically unstable cells exhibit low proliferation in vitro, high proteotoxic stress and deregulated metabolism. However, the intricate relationships that govern the maintenance of cellular homeostasis to ensure the survival of genomically unstable cells remain to be fully explored.

Our group uses quantitative mass spectrometry and modern biochemical methods to understand how cellular homeostasis is modulated in response to genomic instability. We are particularly interested in the roles of autophagy and proteasomal degradation pathways in the maintenance of protein homeostasis in cells with chromosome imbalance. Furthermore, we aim to understand the crosstalk between metabolic reprogramming and genomic instability, and its impact on cell fate determination. The implications of our findings for disease conditions such as cancer and ageing are of interest to us.