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Transcriptional landscape of human myogenesis reavels a key role of TWIST1 in maintenance of skeletal muscle progenitors

ABSTRACT: Transcriptional landscape of human myogenesis reavels a key role of TWIST1 in maintenance of skeletal muscle progenitors

PROVIDER: PRJNA531606 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR8868600_1.fastq.gz	Fastqsanger.gz
	SRR8868600_2.fastq.gz	Fastqsanger.gz
	SRR8868610_1.fastq.gz	Fastqsanger.gz
	SRR8868610_2.fastq.gz	Fastqsanger.gz
	SRR8868591_1.fastq.gz	Fastqsanger.gz

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Transcriptional landscape of human myogenesis reavels a key role of TWIST1 in maintenance of skeletal muscle progenitors

Project description:Derivation of human skeletal muscle in vitro with human pluripotent stem cells (hPSCs) opens new avenues for deciphering essential, but poorly understood aspects of transcriptional regulation in myogenic specification and relevance to rare genetic diseases. We characterized the transcriptional landscape of distinct human myogenic stages, including OCT4::EGFP+ PSCs, MSGN1::EGFP+ presomites, PAX7::EGFP+ skeletal muscle progenitors, MYOG::EGFP+ myoblasts, and multinucleated myotubes. We defined signature gene expression profiles from each population with unbiased clustering analysis, which provided unique insights into the transcriptional dynamics of human myogenesis from undifferentiated hPSCs to fully differentiated myotubes. Using knock-out strategy, we identified TWIST1 as a critical factor in maintenance of human PAX7::EGFP+ putative skeletal muscle progenitors, providing an explanation for the musculoskeletal symptoms of a rare genetic disease, Saethre-Chotzen syndrome. We have established a foundation for future studies to identify regulators of human myogenic ontogeny.

2019-04-10 | GSE129505 | GEO

Transcriptional landscape of myogenesis from human pluripotent stem cells reveals a key role of TWIST1 in maintenance of skeletal muscle progenitors.

Project description:Generation of skeletal muscle cells with human pluripotent stem cells (hPSCs) opens new avenues for deciphering essential, but poorly understood aspects of transcriptional regulation in human myogenic specification. In this study, we characterized the transcriptional landscape of distinct human myogenic stages, including OCT4::EGFP+ pluripotent stem cells, MSGN1::EGFP+ presomite cells, PAX7::EGFP+ skeletal muscle progenitor cells, MYOG::EGFP+ myoblasts, and multinucleated myotubes. We defined signature gene expression profiles from each isolated cell population with unbiased clustering analysis, which provided unique insights into the transcriptional dynamics of human myogenesis from undifferentiated hPSCs to fully differentiated myotubes. Using a knock-out strategy, we identified TWIST1 as a critical factor in maintenance of human PAX7::EGFP+ putative skeletal muscle progenitor cells. Our data revealed a new role of TWIST1 in human skeletal muscle progenitors, and we have established a foundation to identify transcriptional regulations of human myogenic ontogeny (online database can be accessed in http://www.myogenesis.net/).

| S-EPMC6996923 | biostudies-literature

TWIST1

Project description:TWIST1

| PRJNA784600 | ENA

Expression data from myogenesis

Project description:During muscle differentiation, myogenesis sepcific genes are differentially regulated, including Lamins that function at least in maintenance of nuclear architecture and regulation of gene expression. We used microarrays to detail the global changes of gene expression in lamins and nuclear envelope assoicated proteins during myogenesis. Keywords: comparative, myogenesis

2006-04-30 | GSE4694 | GEO

TWIST1 ChIP-seq analysis of human mesenchymal stem cells

Project description:Mesenchymal stem/stromal cells (MSCs) function as skeletal progenitors in bone marrow and regulate hematopoiesis and hemodynamic processes via secretion of paracrine acting factors. Although TWIST1 plays important roles in mesoderm formation and skull and vascular development, its role in MSCs is poorly defined. Therefore, we conducted ChIP-seq analysis to identify genes potentially regulated by TWIST1.

2023-06-01 | GSE220905 | GEO

Neonatal Skeletal Progenitors

Project description:Neonatal Skeletal Progenitors

| PRJNA273968 | ENA

TWIST1 regulated human melanoma transcriptome

Project description:TWIST1 is known to play a role in the metastatic progression of melanoma. However, the range of TWIST1 targets is poorly charachterized. Here microarray analysis was used to define the TWIST1 regulated transcriptome in the human melanoma cell line WM793.

2019-04-03 | GSE128955 | GEO

TWIST1 methylation by SETD6 selectively antagonizes LINC-PINT expression in Glioblastoma multiforme

Project description:Glioblastoma multiforme (GBM) is the most common and aggressive malignant brain tumor among adults, which is characterized by high invasion, migration and proliferation abilities. One important process that contributes to the invasiveness of GBM is the epithelial to mesenchymal transition (EMT). EMT is regulated by a set of defined transcription factors which tightly regulate this process, among them is the basic helix-loop-helix family member, TWIST1. Here we show that TWIST1 is methylated on lysine-33 at chromatin by SETD6, a methyltransferase with expression levels correlating with poor survival in GBM patients. RNA-seq analysis in U251 GBM cells suggested that both SETD6 and TWIST1 regulate cell adhesion and migration processes. We further show that TWIST1 methylation attenuates the expression of the long-non-coding RNA, LINC-PINT, thereby suppressing EMT in GBM. Mechanistically, TWIST1 methylation represses the transcription of LINC-PINT by increasing the occupancy of EZH2 and the catalysis of the repressive H3K27me3 mark at the LINC-PINT locus. Under un-methylated conditions, TWIST1 dissociates from the LINC-PINT locus, allowing the expression of LINC-PINT which leads to increased cell adhesion and decreased cell migration. Together, our findings unravel a new mechanistic dimension for selective expression of LINC-PINT mediated by TWIST1 methylation.

2022-08-12 | PXD029361 | Pride

MyoD-expressing progenitors are essential for skeletal myogenesis and satellite cell development.

Project description:Skeletal myogenesis in the embryo is regulated by the coordinated expression of the MyoD family of muscle regulatory factors (MRFs). MyoD and Myf-5, which are the primary muscle lineage-determining factors, function in a partially redundant manner to establish muscle progenitor cell identity. Previous diphtheria toxin (DTA)-mediated ablation studies showed that MyoD+ progenitors rescue myogenesis in embryos in which Myf-5-expressing cells were targeted for ablation, raising the possibility that the regulative behavior of distinct, MRF-expressing populations explains the functional compensatory activities of these MRFs. Using MyoD(iCre) mice, we show that DTA-mediated ablation of MyoD-expressing cells results in the cessation of myogenesis by embryonic day 12.5 (E12.5), as assayed by myosin heavy chain (MyHC) and Myogenin staining. Importantly, MyoD(iCre/+);R26(DTA/+) embryos exhibited a concomitant loss of Myf-5+ progenitors, indicating that the vast majority of Myf-5+ progenitors express MyoD, a conclusion consistent with immunofluorescence analysis of Myf-5 protein expression in MyoD(iCre) lineage-labeled embryos. Surprisingly, staining for the paired box transcription factor, Pax7, which functions genetically upstream of MyoD in the trunk and is a marker for fetal myoblasts and satellite cell progenitors, was also lost by E12.5. Specific ablation of differentiating skeletal muscle in ACTA1Cre;R26(DTA/+) embryos resulted in comparatively minor effects on MyoD+, Myf-5+ and Pax7+ progenitors, indicating that cell non-autonomous effects are unlikely to explain the rapid loss of myogenic progenitors in MyoD(iCre/+);R26(DTA/+) embryos. We conclude that the vast majority of myogenic cells transit through a MyoD+ state, and that MyoD+ progenitors are essential for myogenesis and stem cell development.

| S-EPMC3838901 | biostudies-literature

TWIST1 is required for HSC maintenance under steady state and stress condition by inhibiting mitochondrial metabolism gene program

Project description:RNA-seq and ATAC-seq were performed to determine possible downstream molecular mechamisms and the changes in chromatin accessibility in long-term hematopoietic stem cell when TWIST1 was absent following irradiation stress. We found that mitochondrial metabolism pathway was strongly turned on in the Twist1-deficient LT-HSCs upon irradiation stress.

2022-06-30 | GSE133682 | GEO

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