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Partnering award helps uncover important embryonic stem cell pathway

16 October 2012

A Japan partnering award from BBSRC has helped enable an international collaboration of researchers to uncover a previously unrecognized regulatory pathway at the heart of embryonic stem (ES) cell biology.

Mouse Embryonic Stem cells (green) re-enter development after being introduced in an early embryo. Credit: Graziano Martello

Mouse Embryonic Stem cells (green) re-enter development after being introduced in an early embryo. Credit: Graziano Martello

ES cells can give rise to every cell type of the body, an ability called pluripotency. For this reason they hold great promise as tools for drug development and regenerative medicine. Crucially, ES cells are able to self-renew - allowing researchers to multiply them in unlimited quantities. How self-renewal is controlled has been something of a mystery.

Now researchers involving teams at the Wellcome Trust - MRC Cambridge Stem Cell Institute, and Dr Hitoshi Niwa from the RIKEN Center for Developmental Biology in Kobe, Japan have found that a transcription factor called Esrrb maintains pluripotency in ES cells and is connected directly to a cellular signaling pathway.

Dr Graziano Martello, who led the study, commented: "These findings expand our understanding of how the behaviour of ES cells is controlled by their environment, bringing us closer to harnessing their potential for medical advances."

This discovery was facilitated by development of new data-mining infrastructure within the Wellcome Trust - MRC Cambridge Stem Cell Institute, which will now be available as a public resource  bioinformatics.cscr.cam.ac.uk/ES_Cell_ChIP-seq_compendium.html.

ENDS

Notes to editors

The collaborative link with Dr Niwa was supported through a BBSRC Japan/UK Partnering Award.

To view the paper, published in October, visit: www.cell.com/cell-stem-cell/abstract/S1934-5909(12)00370-0.

To find out more about BBSRC's Japan Partnering scheme, visit: www.bbsrc.ac.uk/science/international/japan.aspx.

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