Bach1 Regulates the Self-renewal and Mesendodermal Differentiation of Human Embryonic Stem Cells
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE113817 | GEO | 2019/03/28
REPOSITORIES: GEO
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Project description:Human induced pluripotent stem cells (iPS cells) resemble embryonic stem cells and can differentiate into cell derivatives of all three germ layers. However, frequently the differentiation efficiency of iPS cells into some lineages is rather poor. Here, we found that fusion of iPS cells with human hematopoietic stem cells (HSC) enhances iPS cell differentiation. Such iPS hybrids showed a prominent differentiation bias towards hematopoietic lineages but also towards other mesendodermal lineages. Additionally, during differentiation of iPS hybrids expression of early mesendodermal markers - Brachyury (T), MIX1 Homeobox-Like Protein 1 (MIXL1) and Goosecoid (GSC) - appeared with faster kinetics than in parental iPS cells. Following iPS hybrid differentiation there was a prominent induction of NODAL and inhibition of NODAL signaling blunted mesendodermal differentiation. This indicates that NODAL signaling is critically involved in mesendodermal bias of iPS hybrid differentiation. In summary, we demonstrate that iPS cell fusion with HSC prominently enhances iPS differentiation. 11 samples were hybridized GeneChip Human Gene 1.0 ST Arrays (Affymetrix)
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Project description:The epigenome of a cell is established and maintained by chromatin modifiers and remodelers, which are recruited to the chromatin by specific transcription factors. In this report, we show that nodal cross-talks with the epigenome through TRIM33-H3K18ac to mediate mesendodermal genes expression. The chromatin accessibility at mesendodermal genes depends on TRIM33. Moreover, histone acetylation is essential for TRIM33 recruitment to many nodal target genes involved in mesendodermal differentiation. The distribution pattern of the H3K18ac mark changes from foci to expanded domains at the mesendodermal genes promoter during embryonic stem cells (ESCs) differentiation to embryoid bodies (EBs). This could be the cue to facilitate TRIM33 colocalized with Smad2/3 at chromatin in EBs but not in ESCs. TRIM33 interacts with the H3K18ac “writer” p300 dependent on nodal signaling, providing a positive feedback to promote activation of mesendodermal genes and association with HDAC1 plays a negative role in activation of mesendodermal genes.
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Project description:Human induced pluripotent stem cells (iPS cells) resemble embryonic stem cells and can differentiate into cell derivatives of all three germ layers. However, frequently the differentiation efficiency of iPS cells into some lineages is rather poor. Here, we found that fusion of iPS cells with human hematopoietic stem cells (HSC) enhances iPS cell differentiation. Such iPS hybrids showed a prominent differentiation bias towards hematopoietic lineages but also towards other mesendodermal lineages. Additionally, during differentiation of iPS hybrids expression of early mesendodermal markers - Brachyury (T), MIX1 Homeobox-Like Protein 1 (MIXL1) and Goosecoid (GSC) - appeared with faster kinetics than in parental iPS cells. Following iPS hybrid differentiation there was a prominent induction of NODAL and inhibition of NODAL signaling blunted mesendodermal differentiation. This indicates that NODAL signaling is critically involved in mesendodermal bias of iPS hybrid differentiation. In summary, we demonstrate that iPS cell fusion with HSC prominently enhances iPS differentiation.
2014-08-06 | GSE58457 | GEO
Project description:Bach1 Regulates the Self-renewal and Mesendodermal Differentiation of Human Embryonic Stem Cells
| PRJNA454105 | ENA
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis. Examination of BACH1 binding in HEK 293T cells by chromatin immunoprecipitation-sequencing (CHIP-seq) with input DNA as control.
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Project description:This SuperSeries is composed of the following subset Series: GSE28050: Expression data from knockdown of BACH1 in HEK 293T cells GSE28051: Genome-wide map of BACH1 binding in HEK293T cells Refer to individual Series
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Project description:Nodal signaling maintains H3K18ac landscape to promote mesendodermal differentiation through TRIM33
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Project description:Genes regulated by Bach1 transcription factor
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Project description:We identify transcription factor BACH1 as a master regulator in vascular cells during aging. BACH1 is upregulated in the aorta of old mice. We find BACH1 is located on open chromatin and BACH1 binds to CDKN1A gene enhancer and activates its transcription in endothelial cells. Finally, BACH1 aggravates endothelial cell senescence under oxidative stress. Thus, these findings demonstrate a crucial regulatory role of BACH1 in vascular aging.
2024-09-15 | GSE185210 | GEO
Project description:BTB and CNC homology 1 (BACH1) is a heme-binding transcription factor repressing the transcription from a subset of MAF recognition elements (MAREs) at low intracellular heme levels. Upon heme binding, BACH1 is released from the MAREs, resulting in increased expression of antioxidant response genes. To systematically address the gene regulatory networks involving BACH1, we combined chromatin immunoprecipitation-sequencing (ChIP-seq) analysis of BACH1 target genes in HEK 293 cells with knock-down of BACH1 using three independent types of small interfering RNAs followed by transcriptome profiling using microarrays. The 59 BACH1 target genes identified by ChIP-seq were found highly enriched in genes showing expression changes after BACH1 knock-down, demonstrating the impact of BACH1 repression on transcription. In addition to known and new BACH1 targets involved in heme degradation (HMOX1, FTL, FTH1, ME1, SLC48A1) and redox regulation (GCLC, GCLM, SLC7A11), we also discovered BACH1 target genes effecting cell cycle and apoptosis pathways (ITPR2, CALM1, SQSTM1, TFE3, EWSR1, CDK6, BCL2L11, MAFG) as well as subcellular transport processes (CLSTN1, PSAP, MAPT, vault RNA). The newly identified impact of BACH1 on genes involved in neurodegenerative processes and proliferation provides an interesting basis for future dissection of BACH1-mediated gene repression in neurodegeneration and virus-induced cancerogenesis.
2011-05-13 | GSE28051 | GEO