Jennifer Nichols

Dr Jennifer Nichols

Embryonic Pluripotency

Email: jn270@cam.ac.uk

Laboratory Location:

Stem Cell Institute, Gleeson Building

Departmental Affiliation:

Department of Physiology, Development and Neuroscience, University of Cambridge

Co-workers:

Stoyana AlexandrovaThorsten Boroviak Kenneth JonesAgata Kurowski • Carla Mulas

Collaborators: Anne Cooke, Department of Pathology, Cambridge • Kay Elder, Bourn Hall Fertility Clinic, Cambridgeshire • Alfonso Martinez-Arias, Department of Genetics, Cambridge • Berenika Plusa, University of Manchester • Joshua Brickman, University of Edinburgh • Jose Silva, SCI, Cambridge • Austin Smith, SCI, Cambridge

Professional History

Jenny Nichols began her research career with Professor Richard Gardner at the University of Oxford, where she developed a fascination with early mammalian development. She subsequently moved to Edinburgh to join Professor Austin Smith in his newly formed group at the Centre for Genome Research to investigate how the epiblast lineage is established in the embryo and how pluripotent cells can be captured and propagated efficiently in culture as embryonic stem cell lines.

She obtained her PhD in Edinburgh in 1995 and continued as a post doctoral research fellow in Austin Smith's lab until 2006, when she moved to Cambridge to become a group leader under at the SCI.

 


Lab Information 

 

Murine embryos develop a pluripotent epiblast at the late blastocyst stage, which can be propagated in vitro in the form of embryonic stem (ES) cells. The purpose of our research is to discover how the pluripotent cells are assigned, maintained and primed in the embryo. ES cells can be very efficiently derived from murine embryos cultured in the presence of Erk and GSK3 inhibitors, which both prevent differentiation and promote expansion of the epiblast. Although pluripotent cell lines have been derived from other mammals, these differ from murine ES cells, and are more similar to so called ‘epiblast stem cells’ (EpiSCs) derived from post-implantation mouse embryos. 

We are interested in how differences in early embryonic development of various mammalian species influence their subsequent behaviour in culture. We combine functional, molecular and genetic approaches to investigate epiblast development and potential in murine and primate embryos.

Nichols Lab 2014

Human blastocyst donated for research with informed consent, stained for markers of naïve pluripotency: Klf4 is in green, Tfcp2l1 in red and nuclei in blue. Its diameter is around 0.4mm.

Image: Jennifer Nichols

J. Nichols Fig. 1

Fig. 1: Phase image showing a colony of mouse ES cells

J. Nichols Fig. 2

Fig. 2: Confocal image of embryos cultured from the 8 cell stage for two days in control medium (left) and medium supplemented with MEK and GSK3 inhibitors (2i; right). Red staining is Nanog; green staining is Gata4.

Nichols Fig. 3

Fig. 3: Phase image (left) and confocal image (right) of a mouse blastocyst at 4.5 days post coitum showing segregation of inner cell mass into epiblast (red staining for Nanog) and hypoblast (green staining for Gata6)

Plain English

Key Publications

  • Takashima, Y. Guo, G. Loos, R. Nichols, J. Ficz, G. Krueger, F. Oxley, D. Santos, F. Clarke, J. Mansfield, W. Reik, W. Bertone, P. Smith, A. (2014).  Resetting Transcription Factor Control Circuitry toward Ground-State Pluripotency in Human. Cell 158, 1254-69.
  • Boroviak T, Loos R, Bertone P, Smith A, and Nichols J (2014). The ability of inner cell mass cells to self-renew as embryonic stem cells is acquired upon epiblast specification. Nat. Cell Biol. 16, 516-28.
  • Chia G, Muñoz Descalzo S, Kurowski A, Leitch H, Lou X, Mansfield W, Etienne-Dumeau C, Grabole N, Mulas C, Niwa H, Hadjantonakis A. K, and Nichols J (2014).Oct4 is required for lineage priming in the developing inner cell mass of the mouse blastocyst. Development 141, 1001-10.
  •  Betschinger J, Nichols J, Dietmann S, Corrin D, Paddison J and Smith A (2013). Exit from pluripotency is gated by intracellular redistribution of the bHLH transcription factor Tfe3. Cell 153, 335-47.
  • Roode M, Blair K, Snell P, Elder K, Marchant S, Smith A and Nichols J (2012). Human hypoblast formation is not dependent on FGF signalling. Dev. Biol. 361, 358-63 Faculty 1000 ‘Must read’

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