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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 Biology
  • Cancer Institute
  • Faculty of Medical Sciences
 
 
Biography

We are currently seeking a talented bioinformatics post-doc to join the lab. Please see: http://www.ucl.ac.uk/cancer/about_us/vacancies


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 non-coding RNAs function with
transcriptional and chromatin regulators to direct cell differentiation. We have
identified a new class of short RNAs that are transcribed from repressed
polycomb target genes, directly interact with polycomb group proteins and
are depleted upon neuronal differentiation. This work demonstrates
that RNAs can be produced from repressed genes and provides a model for
how polycomb proteins are recruited to chromatin in mammalian cells. To
understand how genes are regulated to control cell fate, we have mapped the
target genes of T cell lineage master regulators 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, AICR, and most recently, an ERC Starting 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 are
currently focused on understanding how new types of non-coding RNAs
function with transcriptional and chromatin regulators to direct cell
differentiation.

We have two main research programmes:

1. Role of non-coding RNAs in polycomb-mediated repression.
Polycomb proteins maintain cell identity by repressing the expression of
developmental regulators specific for other cell types. We have identified
a class of 50-200nt short RNAs transcribed from the beginning of polycomb
target genes in adult T-cells and embryonic stem (ES) cells (Kanhere et
al., 2010). The short RNAs interact with PRC2 through a stem-loop
structure, cause gene repression and are depleted from polycomb target
genes activated during neuronal differentiation. These results support a
role for short RNAs in the association of PRC2 with its target genes. We
are currently exploring the origins and functions of this new class of
RNAs using ES cell and T-cell systems.

2. Transcriptional regulation of CD4+ T-cell differentiation.
CD4+ T helper (Th) cells can differentiate into a number of effector types
that tailor the immune response to different pathogens and we use this
system to understand how genes are regulated to specify different cell types.
We have mapped the binding sites of the Th1 and Th2 master regulators
T-bet and GATA3 in primary human T cells and found that these factors
act through a shared set of target genes (Jenner et al., 2009). More recently, we have discovered that T-bet and GATA3 act through distal sites and that T-bet redistributes GATA3 to different sites in Th1 cells (Kanhere et al., 2012).

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 University College London
2001 MA Master of Arts University of Cambridge
1997 BA Bachelor of Arts University of Cambridge
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