Complementary Activity of ETV5, RBPJ, and TCF3 Drives Formative Transition from Naive Pluripotency

Tüzer Kalkan*, Susanne Bornelöv, Carla Mulas, Evangelia Diamanti, Tim Lohoff, Meryem Ralser, Sjors Middelkamp, Patrick Lombard, Jennifer Nichols, Austin Smith

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

68 Citations (Scopus)

Abstract

The gene regulatory network (GRN)of naive mouse embryonic stem cells (ESCs)must be reconfigured to enable lineage commitment. TCF3 sanctions rewiring by suppressing components of the ESC transcription factor circuitry. However, TCF3 depletion only delays and does not prevent transition to formative pluripotency. Here, we delineate additional contributions of the ETS-family transcription factor ETV5 and the repressor RBPJ. In response to ERK signaling, ETV5 switches activity from supporting self-renewal and undergoes genome relocation linked to commissioning of enhancers activated in formative epiblast. Independent upregulation of RBPJ prevents re-expression of potent naive factors, TBX3 and NANOG, to secure exit from the naive state. Triple deletion of Etv5, Rbpj, and Tcf3 disables ESCs, such that they remain largely undifferentiated and locked in self-renewal, even in the presence of differentiation stimuli. Thus, genetic elimination of three complementary drivers of network transition stalls developmental progression, emulating environmental insulation by small-molecule inhibitors.

Original languageEnglish
Pages (from-to)785-801.e7
JournalCell stem cell
Volume24
Issue number5
DOIs
Publication statusPublished - 2 May 2019

Keywords

  • commitment
  • differentiation
  • embryonic stem cell
  • epiblast
  • ETS factors
  • gene regulatory network
  • pluripotency
  • RBPJ
  • self-renewal

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