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H3K9 tri-methylation at Nanog times differentiation commitment and enables the acquisition of primitive endoderm fate

Abstract : Mouse Embryonic Stem (ES) cells have an inherent propensity to explore distinct gene-regulatory states associated with either self-renewal or differentiation. This property is largely dependent on ERK activity, which promotes silencing of pluripotency genes, most notably of the transcription factor Nanog . Here, we aimed at identifying repressive histone modifications that would mark the Nanog locus for inactivation in response to ERK activity. We found histone H3 lysine 9 tri-methylation (H3K9me3) focally enriched between the Nanog promoter and its −5kb enhancer. While in undifferentiated ES cells H3K9me3 at Nanog depends on ERK activity, in somatic cells it becomes ERK-independent. Moreover, upon deletion of the region harbouring H3K9me3, ES cells display reduced heterogeneity of NANOG expression, delayed commitment into differentiation and impaired ability to acquire a primitive endoderm fate. We suggest that establishment of irreversible H3K9me3 at specific master regulators allows the acquisition of particular cell fates during differentiation.
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Preprints, Working Papers, ...
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https://hal-pasteur.archives-ouvertes.fr/pasteur-03394452
Contributor : Michel Cohen-Tannoudji Connect in order to contact the contributor
Submitted on : Friday, October 22, 2021 - 9:47:15 AM
Last modification on : Tuesday, October 26, 2021 - 4:00:39 AM

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Distributed under a Creative Commons Attribution - NonCommercial - NoDerivatives 4.0 International License

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Agnès Dubois, L. Vincenti, A. Chervova, S. Vandormael-Pournin, Michel Cohen-Tannoudji, et al.. H3K9 tri-methylation at Nanog times differentiation commitment and enables the acquisition of primitive endoderm fate. 2021. ⟨pasteur-03394452⟩

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