A postgraduate research opportunity at the University of Otago.
- Academic background
- Sciences, Health Sciences
- Host campus
- Honours, Master’s, PhD
- Pathology (Dunedin)
- Professor Julia Horsfield
To make a brand new animal from a fertilised egg, two important processes must be integrated. These are (1) cell division for embryo growth, and (2) cell differentiation, in which cells ‘decide what to be’. In the cell division cycle, replicated chromosomes are paired and held together by a protein complex called cohesin. When cells in the embryo differentiate, developmental genes that direct cell type specification must be activated. Research from my group and others found that developmental gene expression also depends on cohesin. This project will test the idea that cohesin’s developmental role involves both cell division and gene expression, which independently inform cell fate decision-making in the embryo.
Because cohesin is a single complex with multiple functions, its subunits and regulators are often assumed to have similar developmental consequences when mutated or depleted. Intriguingly, we found that aberrant gene expression and/or development following depletion of cohesin subunits (or regulators) very much depends on which cohesin protein is depleted and by how much. Our research to date has contributed two important findings to the field: (1) the correct dose of cohesin is important for normal gene expression and development; and that (2) developmental outcomes are likely to derive from more than one of cohesin’s many cellular functions. One view is that cohesin’s developmental role involves regulation of gene expression alone, distinct from its role in cell division. Our hypothesis is that cohesin functions at the nexus of both cell cycle regulation and gene expression to influence the outcome of developmental signalling pathways. No study to date has formally dissected the cell cycle role from the transcriptional role of cohesin in developmental biology, and that is what this project aims to do.