Dr Robert Illingworth; The University of Edinburgh
Whilst studying Molecular Biology at the University of Edinburgh, Rob became fascinated by chemical modifications that could alter the functionality of DNA. This led him to embark on a PhD project with Prof. Adrian Bird to develop novel biochemical tools to isolate DNA based on its methylation status. The timely advent of next generation sequencing provided a means to deep profile these isolates and, in so doing, to produce amongst the first genome-wide DNA methylomes from human and mouse cells. During this early phase of what is now known as ‘genomics’, a lack of analytical tools led Rob to develop novel approaches to explore epigenetic landscapes. Heleveraged this combination of genomics and bioinformatics as a postdoc in the lab of Prof. Wendy Bickmore in the MRC Human Genetics Unit. Here his research focussed on understanding the contribution of polycomb repressive complex 1(PRC1) structural and catalytic functions during early mammalian development. Through this work, Rob started to unpick the requirement for different functions of this essential regulator in the control of developmental gene expression in mammalian cells. In 2018, Rob established his lab in the Centre for Regenerative Medicine (CRM) and the Simon’s Initiative for the Developing Brain (SIDB) in Edinburgh. The Illingworth lab investigates how chromatin-based mechanisms control gene expression programmes to balance the need for cellular expansion and specification, and how derailing these processes leads to pathology.
The fidelity of embryonic development in multicellular organisms relies upon belts and braces control mechanisms to balance the need for cellular expansion and specialisation in time and space. The regulation that underpins this is controlled by transcription factors, that act in concert with context specific chromatin landscapes to control gene transcription. Polycomb proteins; paradigmatic epigenetic co-regulators, operate at the level of chromatin to control master regulators of the pluripotency and developmental programmes. They do so, through the action of functionally related polycomb repressive complexes (PRCs), that modify the chemical and physical properties of chromatin to maintain stable gene silencing. However, the relative contribution of these distinct functions, and their context specificity during development remains largely unknown. To address these questions, our lab utilises pharmacogenetic and synthetic biology approaches to explore how distinct PRC functions regulate gene expression in different cellular and genomic contexts. In this talk I will highlight some of our recent research, focussing in particular on: 1. How impaired PRC activity impacts on cellular specification; 2. The dynamics of how polycomb repression is overcome in response to activating cues; 3. The rules which dictate specific gene activation in response to globally perturbed PRC1 activity.
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