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Snai1 regulates cell lineage allocation and stem cell maintenance in the mouse intestinal epithelium

ABSTRACT: Conditional knockout of Snai1 in the mouse intestinal epithlium results in apoptotic loss of crypt base columnar cells and bias towards differentiation of secretory lineages. In vitro organoid cultures derived from Snail conditional knockout mice also undergo apoptosis when Snai1 is deleted. Snai1 is required for regulation of lineage choice and maintenance of CBC stem cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE65005 | GEO | 2015/02/28

SECONDARY ACCESSION(S): PRJNA272707

REPOSITORIES: GEO

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Snai1 regulates cell lineage allocation and stem cell maintenance in the mouse intestinal epithelium

Project description:Conditional knockout of Snai1 in the mouse intestinal epithlium results in apoptotic loss of crypt base columnar cells and bias towards differentiation of secretory lineages. In vitro organoid cultures derived from Snail conditional knockout mice also undergo apoptosis when Snai1 is deleted. Snai1 is required for regulation of lineage choice and maintenance of CBC stem cells. Total RNA was extracted from organoids cultured for 24 hours after treatment with 0.5ÂµM Tamoxifen derived from Villin-Cre and Villin-Cre, Snai1fl/fl mice.

2015-02-28 | E-GEOD-65005 | biostudies-arrayexpress

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

Project description:In skeletal myogenesis, the transcription factor MyoD, activates distinct transcriptional programs in progenitors compared to terminally differentiated cells. Using ChIP-seq and gene expression analyses, we show that in primary myoblasts, Snai1/2-HDAC1/2 repressive complex bind and exclude MyoD from its targets. Notably, Snail binds E-box motifs that are G/C-rich in their central dinucleotides, and such sites are almost exclusively associated with genes expressed during differentiation. By contrast, Snai1/2 does not bind the A/T-rich E-boxes associated with MyoD targets in myoblasts. Thus, Snai1/2-HDAC1/2 prevents MyoD occupancy on differentiation-specific regulatory elements and the change from Snail1/2- to MyoD-binding often results in enhancer switching during differentiation. Furthermore, we show that a regulatory network involving Myogenic Regulatory Factors (MRFs), Snail/2, miR-30a and miR-206 acts as a molecular switch that controls entry into myogenic differentiation. Together, these results reveal a regulatory paradigm that directs distinct gene expression programs in progenitors versus terminally differentiated cells.

2012-07-05 | GSE38236 | GEO

RNA-seq data of si-Snai1, si-Snai2, si-Snai1/2 and si-Scrambled treated mouse primary myoblasts

2012-07-04 | E-GEOD-38236 | biostudies-arrayexpress

SNAI1 induced epithelial to mesenchymal transition miRNA study in time course

2012-01-13 | GSE35074 | 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). miRNA time series study for 7 times points (4h, 8h, 12h, 24h, 48h, 72h, 96h) in 3 replicates. For each time point, we compared induced and non-induced samples. Overall, we have 42 samples (21 hybridizations).

2012-01-13 | E-GEOD-35074 | biostudies-arrayexpress

Transcription factor Achaete scute-like 2 (Ascl2) controls intestinal stem cell fate

Project description:The small intestinal epithelium is the most rapidly self-renewing tissue of mammals. Proliferative cells are confined to crypts, while differentiated cell types predominantly occupy the villi. We recently demonstrated the existence of a long-lived pool of cycling stem cells defined by Lgr5 expression and intermingled with post-mitotic Paneth cells at crypt bottoms. We have now determined a gene signature for these so called Crypt Base Columnar (CBC) cells. One of the genes within this stem cell signature is the Wnt target Ascl2. Transgenic expression of the Ascl2 transcription factor throughout the intestinal epithelium induces crypt hyperplasia and de novo crypt formation on villi. Induced deletion of the Ascl2 gene in adult small intestine leads to disappearance of the CBC stem cells within days. The combined results from these gain- and loss-of-function experiments imply that Ascl2 controls intestinal stem cell fate. Keywords: expression profiling

2009-03-13 | GSE14201 | GEO

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

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

Loss of SNAI1 induces cellular plasticity in invasive triple-negative breast cancer cells

Project description:To investigate the effect of SNAI1 Knockout on development and growth of triple-negative human breast cancer cells The transcription factor SNAI1 mediates epithelial-mesenchymal transition, fibroblast activation and controls inter-tissue migration. High SNAI1 expression characterizes metastatic triple-negative breast carcinomas, and its knockout by CRISPR/Cas9 uncovered establishment of an epithelio-mesenchymal phenotype accompanied by reduced signaling by the cytokine TGF-β. The SNAI1 knockout cells exhibited plasticity in differentiation, drifting towards the luminal phenotype, gained stemness potential and could differentiate into acinar mammospheres in 3D culture. Loss of SNAI1 derepressed the transcription factor FOXA1, a pioneering factor of mammary luminal progenitors. FOXA1 induced a specific gene program, including the androgen receptor (AR). Inhibiting AR via a specific antagonist regenerated the basal phenotype and blocked acinar differentiation. Thus, loss of SNAI1 in the context of triple-negative breast carcinoma cells promotes an intermediary luminal progenitor phenotype that gains differentiation plasticity, based on the dual transcriptional action of FOXA1 and AR. This function of SNAI1 provides means to separate cell invasiveness from progenitor cell de-differentiation as independent cellular programs.

2022-10-01 | GSE210870 | GEO

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

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