Department of Biochemistry University of Oxford Department of Biochemistry
University of Oxford
South Parks Road
Oxford OX1 3QU

Tel: +44 (0)1865 613200
Fax: +44 (0)1865 613201
Image showing the global movement of lipids in a model planar membrane
Matthieu Chavent, Sansom lab
Anaphase bridges in fission yeast cells
Whitby lab
Lactose permease represented using bending cylinders in Bendix software
Caroline Dahl, Sansom lab
Epithelial cells in C. elegans showing a seam cell that failed to undergo cytokinesis
Serena Ding, Woollard lab
Collage of Drosophila third instar larva optic lobe
Lu Yang, Davis lab
First year Biochemistry students at a practical class
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Neil Brockdorff
Developmental Epigenetics

Co-workers: Dr.Antonio Biasutto, Mr.Joseph Bowness, Dr.Emma Carter, Dr.Jeongyoon Choi, Dr.Heather Coker, Dr.Michal Gdula, Mr.Jonathan Godwin, Dr.Tatyana Nesterova, Miss Lisa Rodermund, Dr.Guifeng Wei, Miss Komal Yasmin, Dr.Tianyi Zhang

Part II Undergraduate Student: Miss Jasmine Rand


Work in the lab centres on understanding the molecular mechanism of X chromosome inactivation, the process mammals use to equalise levels of expression of genes on the X chromosome in females relative to males. X inactivation is initiated by expression of a non-coding RNA, Xist, that coats the chromosome from which it is transcribed, bringing about chromatin modifications that in turn lead to heritable gene silencing. We are interested in how X inactivation is regulated in early development, how X chromosome silencing is established and maintained, and how specific pluripotent lineages can reverse stable silencing of the inactive X.

To address these questions we are combining genetic, cell biological, biochemical and embryology approaches to analyse the role of epigenetic mechanisms such as DNA methylation, RNAi, histone tail modifications, variant histones and chromosome organisation. A central strategy for future work is to identify novel factors involved in epigenetic regulation using both RNAi based loss of function screens and biochemical screens carried out using as bait, factors defined in work to date. Through studying epigenetic mechanisms in X inactivation we aim to better understand their wider role in regulating the genome during differentiation and development.


  1. Pintacuda, G., Wei, G., Roustan, C., Kirmizitas, B.A., Solcan, N., Cerase, A., Castello, A., Mohammed, S., Moindrot, B., Nesterova, T.B. and Brockdorff, N.(2017) hnRNPK Recruits PCGF3/5-PRC1 to the Xist RNA B-Repeat to Establish Polycomb-Mediated Chromosomal Silencing. Molecular Cell 68 955–969
  2. Almeida, M., Pintacuda, G., Masui, O., Koseki, Y., Gdula, M., Cerase, A., Brown, D., Mould, A., Nakayama, M., Schermelleh, L., Nesterova, T.B., Koseki, H., Brockdorff, N. (2017) PCGF3/5-PRC1 initiates Polycomb recruitment in X chromosome inactivation. Science 356 1081-1984 
  3. Cooper, S., Grijzenhout, A., Underwood, E., Ancelin, K., Zhang, T., Nesterova, T.B., Anil-Kirmizitas, B., Bassett, A., Kooistra, S.M., Agger, K., Helin, K., Heard, E., Brockdorff, N. (2016) Jarid2 binds mono-ubiquitylated H2A lysine 119 to mediate crosstalk between Polycomb complexes PRC1 and PRC2. Nature Communications 13661 DOI: 10.1038/ncomms13661
  4. Grijzenhout A., Godwin J., Koseki H., Gdula M., Szumska D., McGouran J.F., Bhattacharya S., Kessler B.M., Brockdorff N., Cooper S. (2016) Functional analysis of AEBP2, a PRC2 Polycomb protein, reveals a Trithorax phenotype in embryonic development and in ES cells. Development 143 2716-2723
  5. Moindrot, B., Cerase, A., Coker, H., Masui, O., Grijzenhout, A., Pintacuda, G., Schermelleh, L., Nesterova, T.B., Brockdorff, N. (2015) A Pooled shRNA Screen Identifies Rbm15, Spen, and Wtap as Factors Required for Xist RNA-Mediated Silencing. Cell Reports 12 562–572
  6. Tavares, L., Dimitrova, E., Oxley, D., Webster, J., Poot, R., Demmers, J., Bezstarosti, K., Taylor, S., Ura, H., Koide, H., Wutz, A., Vidal, M., Elderkin, S., Brockdorff, N. (2012) RYBP-PRC1 complexes mediate H2A ubiquitylation at polycomb target sites independently of PRC2 and H3K27me3. Cell 148 664-678
More Publications...

Research Images

Figure 1: An X;4 translocation chromosome shown at metaphase in which the X component is inactive and on which histone H3 is methylated at lysine 27 (H3K27), and the chromosome 4 component is active with histone H4 being highly acetylated (acH4)


Figure 2: An XX female blastocyst stained for the polycomb repressor protein Eed (green) and the pluripotency marker Oct4, delineating cells of the inner cell mass (red). Foci of Eed staining mark the inactive X chromosome. Western analysis of histones from normal and mutant ES cells demonstrate that the complex containing Eed protein is required for methylation of H3K27 (meK27), but not for histone H2A ubiquitylation (uH2A) which is catalysed by a different polycomb repressor complex


Figure 3: E6.5 mouse embryos with a GFP transgene on the paternal X chromosome illustrate imprinted X inactivation of the paternal X in extraembryonic lineages (left panels, non-green cells). Wholemount RNA FISH reveals Xist RNA domains in an E6.5 XX embryo (central panel). Expanded views illustrate cells in the embryonic and extraembyonic tissues, all of which show Xist RNA domains

Graduate Student and Postdoctoral Positions: Enquiries with CV welcome