The developmental dismantling of pluripotency is reversed by ectopic Oct4 expression

Rodrigo Osorno(MRC Centre for Regenerative Medicine), Anestis Tsakiridis(MRC Centre for Regenerative Medicine), Frederick C.K. Wong(MRC Centre for Regenerative Medicine), Noemí Cambray(MRC Centre for Regenerative Medicine), Constantinos Economou(MRC Centre for Regenerative Medicine), Ronald Wilkie(MRC Centre for Regenerative Medicine), Guillaume Blin(MRC Centre for Regenerative Medicine), Paul J. Scotting(University of Nottingham), Ian Chambers(MRC Centre for Regenerative Medicine), Valerie Wilson(MRC Centre for Regenerative Medicine)
Development
June 5, 2012
Cited by 176Open Access
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Abstract

The transcription factors Nanog and Oct4 regulate pluripotency in the pre-implantation epiblast and in derivative embryonic stem cells. During post-implantation development, the precise timing and mechanism of the loss of pluripotency is unknown. Here, we show that in the mouse, pluripotency is extinguished at the onset of somitogenesis, coincident with reduced expression and chromatin accessibility of Oct4 and Nanog regulatory regions. Prior to somitogenesis expression of both Nanog and Oct4 is regionalized. We show that pluripotency tracks the in vivo level of Oct4 and not Nanog by assessing the ability to reactivate or maintain Nanog expression in cell culture. Enforced Oct4 expression in somitogenesis-stage tissue provokes rapid reopening of Oct4 and Nanog chromatin, Nanog re-expression and resuscitates moribund pluripotency. Our data suggest that decreasing Oct4 expression is converted to a sudden drop in competence to maintain pluripotency gene regulatory network activity that is subsequently stabilized by epigenetic locks.


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