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Identification of a multi-potent Twist2-expressing cell population in the adult heart

ABSTRACT: Identification of a multi-potent Twist2-expressing cell population in the adult heart

PROVIDER: PRJNA485484 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	SRR5388390_1.fastq.gz	Fastqsanger.gz
	SRR5388390_2.fastq.gz	Fastqsanger.gz
	SRR5388381_1.fastq.gz	Fastqsanger.gz
	SRR5388381_2.fastq.gz	Fastqsanger.gz

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Identification of a multi-potent Twist2-expressing cell population in the adult heart (RNA-seq data set)

Project description:Twist transcription factors function as ancestral regulators of mesodermal cell fates in organisms ranging from Drosophlia to mammals. Through lineage tracing of Twist2 (Tw2) expressing cells with tamoxifen-inducible Tw2-CreERT2 and tdTomato reporter mice, we discovered a unique cell population that progressively contributes to multiple cell types in the adult heart, including cardiomyocytes, endothelial cells and fibroblasts. Clonal analysis confirmed the ability of Tw2-derived tdTO+ (Tw2-tdTO+) cells to form CMs in vitro. Within the adult heart, Tw2-tdTO+ cardiomyocytes accounted for ~13% of total cardiomyocytes, the majority of which resulted from fusion of Tw2-tdTO+ cells with existing cardiomyocytes. Tw2-tdTO+ cells also contribute to cardiac remodeling after injury. We conclude that a Tw2-tdTO+ cells participate in lifelong maintenance of cardiac function, at least in part through de novo formation of cardiomyocytes and fusion with preexisting cardiomyocytes, as well as in the genesis of other cellular components of the adult heart.

2020-01-08 | GSE97160 | GEO

Identification of a multi-potent Twist2-expressing cell population in the adult heart (single cell RNA-seq data set)

2020-01-08 | GSE118410 | GEO

Identification of a multi-potent Twist2-expressing cell population in the adult heart (single cell RNA-seq data set)

Project description:Identification of a multi-potent Twist2-expressing cell population in the adult heart (single cell RNA-seq data set)

| PRJNA485493 | ENA

Identification of a multi-potent Twist2-expressing cell population in the adult heart

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-01-08 | GSE118411 | GEO

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

Project description:Integrated analysis of genome-wide ChIP-Seq and RNA-Seq data revealed the first dynamic chromatin and transcriptional landscape of Twist2 binding during myogenic differentiation. During differentiation, Twist2 competes with MyoD at shared DNA motifs to direct global gene transcription and repression of the myogenic program. Additionally, TWIST2 shapes the epigenetic landscape to drive chromatin opening at oncogenic loci and chromatin closing at myogenic loci. These epigenetic changes redirect MyoD binding from myogenic genes towards oncogenic, metabolic, and growth genes.

2019-03-08 | GSE127998 | GEO

Identification of a multipotent Twist2-expressing cell population in the adult heart.

Project description:Twist transcription factors function as ancestral regulators of mesodermal cell fates in organisms ranging from Drosophila to mammals. Through lineage tracing of Twist2 (Tw2)-expressing cells with tamoxifen-inducible Tw2-CreERT2 and tdTomato (tdTO) reporter mice, we discovered a unique cell population that progressively contributes to cardiomyocytes (CMs), endothelial cells, and fibroblasts in the adult heart. Clonal analysis confirmed the ability of Tw2-derived tdTO+ (Tw2-tdTO+) cells to form CMs in vitro. Within the adult heart, Tw2-tdTO+ CMs accounted for ∼13% of total CMs, the majority of which resulted from fusion of Tw2-tdTO+ cells with existing CMs. Tw2-tdTO+ cells also contribute to cardiac remodeling after injury. We conclude that Tw2-tdTO+ cells participate in lifelong maintenance of cardiac function, at least in part through de novo formation of CMs and fusion with preexisting CMs, as well as in the genesis of other cellular components of the adult heart.

| S-EPMC6130356 | biostudies-literature

Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

Project description:Genome-wide maps of Twist2-binding, MyoD-binding and chromatin state in Twist2-overexpressing Twist2+ cells

| PRJNA526023 | ENA

Abcg2 expressing VESC in adult heart

Project description:Abcg2 expressing VESC in adult heart

| PRJNA938150 | ENA

Regulation of p21 by TWIST2 contributes to its tumor suppressor function in human acute myeloid leukemia

Project description:TWIST2 is deregulated in about 1/3 human acute myeloid leukemia (AML)M-BM- patients partially due to hypermethylation. Overexpression of TWIST2 in various AML cell lines and primary AML cells leads to growth arrest, reduced colony forming cell (CFC) capacity, inhibited cell migration and tumorigenic ability in nude mice, suggesting its tumor suppressor role in AML. To explore the molecular insight of how TWIST2 acts as a tumor suppressor in AML cells, control and TWIST2 expressed THP-1 cells have been analyzed with microarray. 4 independent biological replicates of control and TWIST2 expressed THP-1 cells have been used for RNA extraction and microarray analysis with Agilent platform.

2014-05-07 | E-GEOD-57347 | biostudies-arrayexpress

TWIST2-Mediated Chromatin Remodeling Promotes Fusion-Negative Rhabdomyosarcoma [ChIP-seq]

Project description:Sarcomas are derailed in pathways that specify mesenchymal lineages during embryogenesis, causing tumor cells to stall at early stages of differentiation. Among them, rhabdomyosarcoma (RMS) is a pediatric soft tissue sarcoma of skeletal muscle origin. A key feature of RMS is their inability to terminally differentiate despite the high expression of master myogenic regulator MYOD. The bHLH transcription factor TWIST2, which governs mesenchymal stem cell identity and restricts myogenesis, is overexpressed in patient fusion-negative RMS (FN-RMS) tumors. We show that knockdown of TWIST2 enables FN-RMS cells to exit the cell cycle and undergo myogenic differentiation, thereby reducing the growth of FN-RMS xenograft tumors. ChIP-seq analysis revealed that most TWIST2-mediated gene regulation occurs independent of changes in MYOD binding in FN-RMS cells. Instead, TWIST2 controls the deposition of H3K27 acetylation at distal enhancers by interacting with the chromatin remodelers, SMARCA4 and CHD3, to activate growth-related and repress myogenesis-related TWIST2 target genes. Our findings provide new insights into the role of TWIST2 in maintaining an undifferentiated and tumorigenic state of FN-RMS and highlight the clinical potential of reversing the TWIST2-regulated phenotype.

2023-03-20 | GSE207165 | GEO

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