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Dr Richard Jenner
534D
UCL Cancer Institute, Paul O'Gorman Building
72 Huntley Street
London
WC1E 6BT
Tel: 020 7679 6815
Fax: 020 7209 0470
Appointment
  • Reader in Molecular Biology
  • Research Department of Cancer Bio
  • Cancer Institute
  • Faculty of Medical Sciences
Biography

Each of our cells contains the same copy of our genome but it is how distinct parts of the genome are accessed in different cells that allows embryogenesis to proceed and for specialised cell types to emerge and be maintained. Defects in this process can lead to developmental disorders, immunodeficiency and cancer. The overall aim of our lab is to understand how access to the genome is controlled during cell differentiation. 


We are currently focused on understanding how interactions between chromatin regulators and RNA function to direct cell differentiation. Polycomb repressive complex 2 (PRC2) is critical for development and the maintenance of cell identity and its function is often perturbed in cancer. PRC2 functions to modify chromatin to maintain genes specific for other cell types in a repressed state. We have recently discovered that PRC2 interacts with nascent RNA at active genes and this functions to prevent PRC2 from inappropriately silencing gene expression. 

We are also interested in how master regulator transcription factors, which dictate the developmental fate of cells, function to control gene expression. Using lineage specification of T helper cells as a model, we have mapped the target genes of the Th1 and Th2 master regulators T-bet and GATA3 across the genome and are continuing to use this as a model system to understand the control of cell differentiation.

Previously, I was awarded a BA in Natural Sciences at the University of Cambridge and I completed my Ph.D. thesis with Paul Kellam and Chris Boshoff at UCL profiling viral and host gene expression in human B-cell lymphoma. I then moved to the US as a postdoctoral associate in Rick Young’s lab at the Whitehead Institute where I applied ChIP-Chip technology to determine how polycomb maintains ES cell pluripotency and how NF-kappaB coordinates the transcriptional response to infection. I returned to UCL as a MRC Career Development Fellow in 2006 and have since been awarded further funding from the Wellcome Trust, NIHR, EMBO, Worldwide Cancer Research and an ERC Consolidator Grant.

Research Summary

Each of our cells contains the same copy of our genome but - it is how distinct parts of the genome are accessed in different cells that allows embryogenesis to proceed and for specialised cell types to emerge and be maintained. Defects in this process can lead to developmental disorders,  immunodeficiency and cancer. The overall aim of our lab is to understand how access to the genome is controlled during cell differentiation. 


We have two main research programmes:

1. Role of RNA in chromatin and transcriptional regulation.

Polycomb repressive complex 2 (PRC2) is critical for development and the maintenance of cell identity and its function is often perturbed in cancer. PRC2 functions to modify chromatin to maintain genes specific for other cell types in a repressed state. The determinants responsible for the pattern in which PRC2 is recruited to chromatin are still not fully understood.

In addition to its association with chromatin, we and others have shown that PRC2 also interacts with RNA (Kanhere et al., 2010). PRC2 interacts with nascent RNAs at protein-coding genes and with long non-coding RNAs and a number of studies have suggested that RNA functions in the recruitment of PRC2 to chromatin. However, the set of RNAs directly bound by PRC2 in living cells, the PRC2 subunits that mediate these interactions, and the role of RNA in the recruitment of PRC2 to chromatin have remained unclear.

We have recently applied iCLIP to identify the RNAs directly bound by endogenous PRC2 in ES cells (Beltran et al., 2016). We discovered that PRC2 interacts with nascent RNA at essentially all active genes. Using genetic tools, measurements of PRC2 chromatin interaction upon RNA degradation, and in vitro PRC2-nucleosome binding assays, we have also revealed that the interaction of PRC2 with RNA or chromatin is mutually antagonistic. This suggests that RNA prevents PRC2 recruitment to chromatin at active genes and that mutual antagonism between RNA and chromatin underlies the pattern of PRC2 chromatin association across the genome.

2. Transcriptional regulation of T helper cell differentiation.

A second major interest of the lab is understanding how master regulator transcription factors, function to dictate the developmental fate of cells. CD4+ T helper (Th) cells can differentiate into a number of specialised lineages that tailor the immune response to specific pathogens and to cancer. Defects in this process can lead to immunodeficiency, autoimmunity or allergies. Th cell lineage specification is controlled by a set of master regulator transcription factors. We have mapped the binding sites of the Th1 and Th2 master regulators T-bet and GATA3 across the genome and have discovered that T-bet and GATA3 act through a shared set of distal sites and that T-bet blocks Th2 cell differentiation by sequestering GATA3 away from Th2 genes and redistributing it to Th1 sites (Jenner et al., 2009; Kanhere et al., 2012; Evans and Jenner, 2014). We are continuing to use this system as a model to probe the mechanisms through which master regulator transcription factors function.

Teaching Summary

I lecture on the UCL MSc courses in Infection and Immunity and Cancer and the Intercalated BSc in Immunology, Infection & Cell Pathology.

Academic Background
2003 PhD Doctor of Philosophy – Molecular Biology University College London
2001 MA Master of Arts – Natural Sciences University of Cambridge
1997 BA Bachelor of Arts – Natural Sciences University of Cambridge
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