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Id1 maintains embryonic stem cell self-renewal by upregulation of Nanog and repression of Brachyury expression

ABSTRACT: Understanding the mechanism by which embryonic stem (ES) cells self-renew is critical for the realization of their therapeutic potential. Previously it had been shown that in combination with LIF, Id proteins were sufficient to maintain mouse ES cells in a self-renewing state. Here we investigate the requirement for Id1 in maintaing ES cell self-renewal and blocking differentiation. We find that Id1-/- ES cells have a propensity to differentiate and a decreased capacity to self-renew. Chronic or acute loss of Id1 leads to a down-regulation of Nanog, a critical regulator of self-renewal. In addition, in the absence of Id1, ES cells express elevated levels of Brachyury, a marker of mesendoderm differentiation. We find that loss of both Nanog and Id1 is required for the up-regulation of Brachyury, and Id1 maintains Nanog expression by blocking the expression of Zeb1, a repressor of Nanog transcription. These results identify Id1 as an important factor in the maintenance of ES cell self-renewal and suggest a plausible mechanism for its control of lineage commitment.

ORGANISM(S): Mus musculus

PROVIDER: GSE19144 | GEO | 2011/11/01

SECONDARY ACCESSION(S): PRJNA120693

REPOSITORIES: GEO

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Id1 maintains embryonic stem cell self-renewal by upregulation of Nanog and repression of Brachyury expression

Project description:Understanding the mechanism by which embryonic stem (ES) cells self-renew is critical for the realization of their therapeutic potential. Previously it had been shown that in combination with LIF, Id proteins were sufficient to maintain mouse ES cells in a self-renewing state. Here we investigate the requirement for Id1 in maintaing ES cell self-renewal and blocking differentiation. We find that Id1-/- ES cells have a propensity to differentiate and a decreased capacity to self-renew. Chronic or acute loss of Id1 leads to a down-regulation of Nanog, a critical regulator of self-renewal. In addition, in the absence of Id1, ES cells express elevated levels of Brachyury, a marker of mesendoderm differentiation. We find that loss of both Nanog and Id1 is required for the up-regulation of Brachyury, and Id1 maintains Nanog expression by blocking the expression of Zeb1, a repressor of Nanog transcription. These results identify Id1 as an important factor in the maintenance of ES cell self-renewal and suggest a plausible mechanism for its control of lineage commitment. Wild type and Id1-/- ES cells were grown on gelatin under normal self-renewing conditions (in the presence of serum and LIF).

2011-11-01 | E-GEOD-19144 | biostudies-arrayexpress

Mus musculus

Project description:Id1 maintains embryonic stem cell self-renewal by upregulation of Nanog and repression of Brachyury expression

| PRJNA120693 | ENA

Transcriptomic profiling of 4T1 cells depleted for Id1/3 and Robo1

Project description:Id1 and its closely related family member Id3 are expressed by a diversity of stem and progenitor cells. We show that Id1/3 are required for the self-renewal and proliferation of triple negative breast cancer (TNBC) cells both in vitro and in vivo. Furthermore, we identified that Id1/3 negatively regulates the tumour suppressor gene Robo1. Depletion of Robo1 could rescue the proliferative defect induced by Id1/3 knockdown. To understand the mechanisms by which Robo1 rescues cell proliferation in Id1/3 depleted cells, we performed RNA-Sequencing on 4T1 cells with Dox-inducible Id1/3 KD and/or Robo1 depletion using siRNA. We conclude that following Id1/3 knockdown, Robo1 is induced and exerts anti-proliferative effects via suppression of a Myc transcriptional program.

2020-10-31 | GSE129858 | GEO

Function of deubiquitinase USP21 in mouse embryonic stem cell [RNA-Seq]

Project description:Ubiquitination-mediated protein degradation of key transcriptional factors is important to the self-renewal of embryonic stem (ES) cells. However, little is known about the deubiquitination in ES self-renewal and differentiation. Here, we report that deubiquitinase USP21 is an important positive regulator to keep ES cells under undifferentiation stasus by deubiquitination and stabilization of Nanog, a key transcriptional factor of ES cells. Loss of USP21 led to ES cells differentiation and defect in reprogramming.

2016-10-05 | GSE69987 | GEO

FGF2 sustains NANOG and switches the outcome of BMP4 induced human embryonic stem cell differentiation

Project description:NANOG has emerged as a central gatekeeper of pluripotency. Here we show that as human embryonic stem (ES) cells exit the pluripotent state, NANOG can play a key role in determining lineage outcome. It has previously been reported that BMPs can induce differentiation of human ES cells into extraembryonic lineages. Here we report that FGF2 switches BMP4 induced differentiation outcome to mesendoderm, characterized by the uniform expression of T (brachyury) and other primitive streak markers. Blocking the MEK-ERK pathway either by chemical inhibitors or by an ERK-specific phosphatase (DUSP6) blocks the FGF2-mediated lineage switch. Active MEK-ERK signaling prolongs NANOG expression during BMP-induced differentiation. Forced NANOG expression results in FGF independent BMP4 induction of mesendoderm, and knockdown of NANOG greatly reduces T induction. Together, our results demonstrate that FGF2 signaling switches the outcome of BMP4 induced differentiation of human ES cells by maintaining NANOG levels through the MEK-ERK pathway.

2011-03-03 | GSE25973 | GEO

FGF2 sustains NANOG and switches the outcome of BMP4 induced human embryonic stem cell differentiation

2011-03-03 | E-GEOD-25973 | biostudies-arrayexpress

Quantitative analysis of Id1 Wild Type and Id1 knockout hematopoietic stem cells transcriptome

Project description:To explore the molecular basis by which Id1 loss promotes HSC quiescence under stress we compared the transcriptome of Id1-/- and Id1+/+ HSCs isolated from primary BMT recipient mice by RNA-seq. We found 179 upregulated and 1476 downregulated genes in Id1-/- HSCs compared to Id1+/+ HSCs using a fold-change cut-off of 2 . Collectively, the IPA analysis shows that Id1-/- HSCs have gene expression profiles consistent with reduced response to stress, reduced cycling and proliferation, and reduced ribosomal biogenesis and protein synthesis, which is consistent with our hypothesis that Id1-/- HSCs have molecular signature of quiescent HSCs compared to Id1+/+ HSCs.

2018-08-09 | GSE114533 | GEO

Gene expression analysis of subpopulations of mouse embryonic stem cells sorted based on Id1 and Nanog expression

Project description:Analysis of gene expression in sorted subpopulations of mouse embryonic stem cells. We set out to investigate whether expression of Id1 in Nanog-low cells affected the expression of pluripotency factors and signalling molecules.

2018-12-15 | GSE108226 | GEO

Sall4 regulates distinct transcription circuitries in different blastocyst-derived stem cell lineages

Project description:Stem cells self-renew or differentiate under the governance of a stem cell-specific transcriptional program with each transcription factor orchestrating the activities of a particular set of genes. Here we demonstrate that a single transcription factor is able to regulate distinct core circuitries in two different blastocyst-derived stem cell lines, embryonic stem (ES) and extra-embryonic endoderm (XEN) cells. The transcription factor, Sall4, is required for early embryonic development and for ES cell pluripotency. Sall4 is also expressed in XEN cells and depletion of Sall4 disrupts self-renewal and induces differentiation. Genome-wide analysis reveals Sall4 is regulating different gene sets in ES and XEN cells, and depletion of Sall4 targets in the respective cell types induces differentiation. With Oct4, Sox2 and Nanog, Sall4 forms a crucial interconnected auto-regulatory network in ES cells. In XEN cells, Sall4 regulates key XEN lineageassociated genes, Gata4, Gata6, Sox7 and Sox17. Our findings demonstrate how Sall4 functions as an essential stemness factor for two different stem cell lines. Keywords: ES/XEN comparison, ES Sall4 KD/control KD comparison, and XEN Sall4 KD/control KD comparison

2008-08-19 | GSE12482 | GEO

Wdr5 mediates self-renewal and reprogramming via the embryonic stem cell core transcriptional network

Project description:The embryonic stem (ES) cell transcriptional and epigenetic networks are critical for the maintenance of ES cell self-renewal. However, it remains unclear whether components of these networks functionally interact and if so, what factors mediate such interactions. Here we show that WD-repeat protein-5 (Wdr5), a core member of the mammalian Trithorax (trxG) complex, positively correlates with the undifferentiated state and is a novel regulator of ES cell self-renewal. We demonstrate that Wdr5, an ‘effector’ of H3K4 methylation, interacts with the pluripotency transcription factor Oct4. In concordance, genome-wide ChIP-Seq and transcriptome analyses demonstrate overlapping gene regulatory functions between Oct4 and Wdr5. We show that the Oct4-Sox2-Nanog circuitry cooperates with trxG for transcriptional activation of key self-renewal regulators. Furthermore, Wdr5 expression is required for the efficient formation of induced pluripotent stem (iPS) cells. Collectively, these findings implicate an integrated model of transcriptional and epigenetic control, mediated by select trxG members, for the maintenance of ES cell self-renewal and somatic cell reprogramming. 7 Samples

2011-04-08 | E-GEOD-22934 | biostudies-arrayexpress

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