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Retinoic acid induces Snai1 in stem cells of the preimplantation blastocyst to initiate differentiation

ABSTRACT: Although much is known about the pluripotency self-renewal circuitry, the molecular events that lead embryonic stem cells (ESCs) exit from pluripotency and begin differentiation are largely unknown. We found that the zinc finger transcription factor Snai1, involved in gastrulation and epithelial- mesenchymal transition (EMT) is already expressed in the inner cell mass of the preimplantation blastocysts. In ESCs Snai1 does not respond to TGFα or BMP4 signalling but it is induced by retinoic acid (RA) treatment, which induces the binding, on the Snai1 promoter, of the retinoid receptors RARγ and RXRα the dissociation of the Polycomb repressor compex 2 (PRC2) which results in the decrease of H3K27me3 and the increase of histone H3K4me3. Snai1 mediates the repression of pluripotency genes by binding directly to the promoters of Nanog, Nr5a2, Tcl1, c-Kit, and Tcfcp2l1. The transient activation of Snai1 in embryoid bodies induces the expression of the markers of all three germ layers. These results suggest that Snai1 is a key factor that triggers ESCs exit from the pluripotency state and initiate their differentiation processes.

ORGANISM(S): Mus musculus

PROVIDER: GSE57854 | GEO | 2015/01/12

SECONDARY ACCESSION(S): PRJNA248261

REPOSITORIES: GEO

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Retinoic acid induces Snai1 in stem cells of the preimplantation blastocyst to initiate differentiation

Project description:Although much is known about the pluripotency self-renewal circuitry, the molecular events that lead embryonic stem cells (ESCs) exit from pluripotency and begin differentiation are largely unknown. We found that the zinc finger transcription factor Snai1, involved in gastrulation and epithelial- mesenchymal transition (EMT) is already expressed in the inner cell mass of the preimplantation blastocysts. In ESCs Snai1 does not respond to TGFÎ± or BMP4 signalling but it is induced by retinoic acid (RA) treatment, which induces the binding, on the Snai1 promoter, of the retinoid receptors RARÎ³ and RXRÎ± the dissociation of the Polycomb repressor compex 2 (PRC2) which results in the decrease of H3K27me3 and the increase of histone H3K4me3. Snai1 mediates the repression of pluripotency genes by binding directly to the promoters of Nanog, Nr5a2, Tcl1, c-Kit, and Tcfcp2l1. The transient activation of Snai1 in embryoid bodies induces the expression of the markers of all three germ layers. These results suggest that Snai1 is a key factor that triggers ESCs exit from the pluripotency state and initiate their differentiation processes. microarray analysis of embryonic stem cells (ESC) expressing Snail-ER at various time points of induction with 4-OHT

2015-01-12 | E-GEOD-57854 | biostudies-arrayexpress

Expression data from control and Snai1 knockout embryonic stem cells (ESCs)

Project description:Snail1 is a master epithelial-mesenchymal trisition (EMT) factor but its role in ESC maintenance is unknown. We used microarrays to compare the global gene expression between control and Snai1 knockout ESCs. RNA extracted from control and Snai1 knockout ESCs were hybridizated on Affymetrix microarrays.

2013-12-10 | E-GEOD-53107 | biostudies-arrayexpress

Expression data from control (F/F) and Snai1 knockout (KO) embryoid body (EB) and teratoma ™

Project description:Snai1 is a master factor of epithelial to mesenchymal transitioin (EMT), however, its role in embryonic stem cell (ESC) differentiation and lineage commitment remains undefined. We used microarrays to compare the global programme of gene expression between control and Snai1 knockout ESCs-derived EB and teratoma. For EBs, control and Snai1 knockout ESCs were cultured as embryoid bodies in spotaneous differentiation media, RNA of 5 days EBs were collected for Affymetrix microarrays. For teratomas, control and Snai1 knockout ESCs were injected into nude mice to form teratomas. RNA of 6 weeks were collected for Affymetrix microarrays.

2013-12-10 | E-GEOD-53106 | biostudies-arrayexpress

Expression data of control (F/F) and Snai1 knockout (KO) Flk1+/- cells

Project description:Snai1 is a master factor of epithelial to mesenchymal transitioin (EMT), however, its role in embryonic stem cell (ESC) differentiation and lineage commitment remains undefined. We used microarrays to compare the global programme of gene expression between control and Snai1 knockout Flk1+ and Flk1- cells sorted from 4 day EBs. Control and Snai1 knockout ESCs were cultured as embryoid bodies in spotaneous differentiation media, 4 days EBs were dissociated and sorted by anti-Flk1 antibody to separated Flk1+ and Flk1- cells, total RNA were collected for Affymetrix microarrays

2013-12-10 | E-GEOD-53108 | biostudies-arrayexpress

Expression data from control (F/F) and Snai1 knockout (KO) embryoid body (EB) and teratoma ™

2013-12-10 | GSE53106 | GEO

Expression data from control and Snai1 knockout embryonic stem cells (ESCs)

2013-12-10 | GSE53107 | GEO

SNAI1 induced epithelial to mesenchymal transition miRNA study in time course

Project description:To identify miRNAs participating in SNAI1-orchestrated regulatory pathways, we analysed time-resolved microarray data of SNAI1-induced EMT, obtained during conditional expression of SNAI1 in a “Tet-Off” MCF7-SNAI1 breast carcinoma cell model (Vetter et al, 2009).

2012-01-13 | GSE35074 | GEO

SNAI1 knockdown under VEGF stimulus in HUVECs

Project description:The goal of this study was to reveal SNAI1 function in angiogenesis. SNAI1 is up-regulated by VEGF stimulus. Using RNASeq method (single-ended 150-bp sequencing on Illumina Hi-seq 3000 instrument), we measured the transcriptional difference between siSNAI1 or NC-transfected HUVECs.

2019-03-04 | GSE111386 | GEO

Jun-mediated changes in cell adhesion contribute to embryonic stem cell exit from ground state pluripotency

Project description:Embryonic stem cells (ESC) are able to give rise to any somatic cell type. A lot is known about how ESC pluripotency is maintained, but comparatively less is known about how differentiation is promoted. Cell fate decisions are regulated by interactions between signalling and transcriptional networks. Recent studies have shown that the overexpression or downregulation of the transcription factor Jun can affect the ESC fate. Here we have focussed on the role of the Jun in the exit of mouse ESCs from ground state pluripotency and the onset of early differentiation. Transcriptomic analysis of differentiating ESCs reveals that Jun is required to upregulate a programme of genes associated with cell adhesion as ESCs exit the pluripotent ground state.

2015-12-07 | E-MTAB-4068 | biostudies-arrayexpress

Mitotic bookmarking redundancy by nuclear receptors mediates robust post-mitotic reactivation of the pluripotency network.

Project description:Mitotic bookmarking transcription factors (TFs) are thought to mediate rapid and accurate post-mitotic gene reactivation. However, the loss of individual bookmarking TFs often leads to the deregulation of only a small proportion of their mitotic targets, raising doubts on the significance and importance of their bookmarking function. Here, we used targeted proteomics of the mitotic bookmarking TF ESRRB, an orphan nuclear receptor, to discover an unexpected redundancy among members of the protein superfamily of nuclear receptors. Focusing on the nuclear receptor NR5A2, which together with ESRRB is essential in maintaining pluripotency in mouse embryonic stem cells, we demonstrate conjoint bookmarking activity of both factors on promoters and enhancers of a large fraction of active genes, particularly the most rapidly and strongly reactivated ones. Upon fast and simultaneous degradation of both factors during mitotic exit, hundreds of mitotic targets of ESRRB/NR5A2, including key players of the pluripotency network, display attenuated transcriptional reactivation. We propose that redundancy in mitotic bookmarking TFs, especially nuclear receptors, confers robustness to the reestablishment of gene regulatory networks after mitosis.

2023-11-20 | PXD038950 | Pride

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