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Bach1 Regulates the Self-renewal and Mesendodermal Differentiation of Human Embryonic Stem Cells

ABSTRACT: Bach1 Regulates the Self-renewal and Mesendodermal Differentiation of Human Embryonic Stem Cells

PROVIDER: PRJNA454105 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7079900_1.fastq.gz	Fastqsanger.gz
	SRR7079900_2.fastq.gz	Fastqsanger.gz
	SRR7079901_1.fastq.gz	Fastqsanger.gz
	SRR7079901_2.fastq.gz	Fastqsanger.gz
	SRR7079902_1.fastq.gz	Fastqsanger.gz

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Bach1 Regulates the Self-renewal and Mesendodermal Differentiation of Human Embryonic Stem Cells

Project description:Transcription factor Bach1 is a member of the alkaline leucine zipper protein family. Our results therefore highlight a critical role for Bach1 proteins in a regulatory network that integrates essential Wnt/β-catenin and nodal-Smad signaling to repress mesendodermal differentiation of pluripotent cells

2019-03-28 | GSE113817 | GEO

BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells

Project description:The relationship between enhancer region chromatin accessibility of the Leukemia Inhibitory Factor Receptor (Lifr) gene and the regulation of self-renewal in mouse embryonic stem cells (mESCs)remains poorly understood. In this study, we elucidate the BACH1 enhances the activity of Lifr enhancer by recruiting STAT3 and activates the LIFR-STAT3 signaling pathway by promoting the LIFR expression, thereby maintaining the self-renewal of mESCs. Our results complement a novel insight into the regulatory role of BACH1 in maintaining the self-renewal capacity of mESCs.

2025-07-19 | GSE299206 | GEO

BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells [ChIP-seq]

2025-07-19 | GSE299411 | GEO

Bach1 regulates self-renewal and impedes mesendodermal differentiation of human embryonic stem cells.

Project description:The transcription factor BTB and CNC homology 1 (Bach1) is expressed in the embryos of mice, but whether Bach1 regulates the self-renewal and early differentiation of human embryonic stem cells (hESCs) is unknown. We report that the deubiquitinase ubiquitin-specific processing protease 7 (Usp7) is a direct target of Bach1, that Bach1 interacts with Nanog, Sox2, and Oct4, and that Bach1 facilitates their deubiquitination and stabilization via the recruitment of Usp7, thereby maintaining stem cell identity and self-renewal. Bach1 also interacts with polycomb repressive complex 2 (PRC2) and represses mesendodermal gene expression by recruiting PRC2 to the genes' promoters. The loss of Bach1 in hESCs promotes differentiation toward the mesendodermal germ layers by reducing the occupancy of EZH2 and H3K27me3 in mesendodermal gene promoters and by activating the Wnt/β-catenin and Nodal/Smad2/3 signaling pathways. Our study shows that Bach1 is a key determinant of pluripotency, self-renewal, and lineage specification in hESCs.

| S-EPMC6415956 | biostudies-literature

IGF1-mediated human embryonic stem cell self-renewal recapitulates the embryonic niche

Project description:IGF1-mediated human embryonic stem cell self-renewal recapitulates the embryonic niche

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Zfx controls self-renewal of human embryonic stem cells

Project description:Previously, we identified the transcription factor Zfx as a key regulator of self-renewal in murine ESCs. Here we extend those findings to human ESCs. Zfx knockdown in hESCs hindered clonal growth and decreased colony size after serial replating. Zfx overexpression enhanced clone formation, increased colony size and decreased expression of differentiation-related genes in human ESCs. Zfx-overexpressing hESCs resisted spontaneous differentiation but could be directed to differentiate into endodermal and neural cell fates when provided with the appropriate cues. Thus, Zfx acts as a molecular rheostat regulating the balance between self-renewal and differentiation in hESCs, revealing the close evolutionary conservation of the self-renewal mechanisms in murine and human ESCs. Human embryonic stem cells with over expression of ZFX were compared to the original cell line (H9) and a clonally derived wild-type cell line (clone 3)

2012-01-01 | E-GEOD-29784 | biostudies-arrayexpress

Zfx controls the self-renewal of embryonic and hematopoietic stem cells

Project description:Stem cells (SC) exhibit a unique capacity for self-renewal in an undifferentiated state. It is unclear whether the self-renewal of pluripotent embryonic SC (ESC) and of tissue-specific adult SC such as hematopoietic SC (HSC) is controlled by common mechanisms. The deletion of transcription factor Zfx impaired the self-renewal but not the differentiation capacity of murine ESC; conversely, Zfx overexpression facilitated ESC self-renewal by opposing differentiation. Furthermore, Zfx deletion abolished the maintenance of adult bone marrow HSC, but did not affect erythromyeloid progenitors or fetal HSC. In both ESC and HSC, Zfx activated a common set of direct target genes. In addition, the loss of Zfx resulted in the induction of immediate-early and/or stress-inducible genes in both SC types but not in their differentiated progeny. These studies identify the first shared transcriptional regulator of ESC and HSC, suggesting a common molecular basis of self-renewal in embryonic and adult SC. Keywords: Global gene expression data analysis in Zfx-deficient murine ESC and HSC

2007-04-20 | GSE7069 | GEO

Lineage-specific enhancers activate self-renewal genes in macrophages and embryonic stem cells

Project description:Differentiated macrophages can self-renew in tissues and expand long-term in culture, but the gene regulatory mechanisms that accomplish self-renewal in the differentiated state have remained unknown. Here we show that in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire associated with a gene network controlling self-renewal. Single cell analysis revealed that, in vivo, proliferating resident macrophages can access this network by transient down-regulation of Maf transcription factors. The network also controls embryonic stem cell self-renewal but is associated with distinct embryonic stem cell-specific enhancers. This indicates that distinct lineage-specific enhancer platforms regulate a shared network of genes that control self-renewal potential in both stem and mature cells.

2016-02-03 | GSE75722 | GEO

BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells

Project description:BACH1 recruits STAT3 to enhance leukemia inhibitory factor receptor activity and augments the self-renewal capacity of mouse embryonic stem cells

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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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