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ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes

ABSTRACT: ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes

PROVIDER: PRJNA473586 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7232000_1.fastq.gz	Fastqsanger.gz
	SRR7232000_2.fastq.gz	Fastqsanger.gz
	SRR7232001_1.fastq.gz	Fastqsanger.gz
	SRR7232001_2.fastq.gz	Fastqsanger.gz
	SRR7231996_1.fastq.gz	Fastqsanger.gz

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ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes

Project description:ETV1 (ER81) was identified as a highly enriched transcription factor in rapidly conducting atrial and His-Purkinje cardiomyocytes. Previous work has shown that ETV1 is a critical factor in determining fast conduction physiology in the heart. This high-throughput sequencing project aims to uncover ETV1-dependent gene networks in cardiomyocytes. These results provide insight into the role of ETV1 in the establishment of rapid conduction zones in the heart.

2018-10-15 | GSE115061 | GEO

ETV1 activates a rapid conduction transcriptional program in rodent and human cardiomyocytes.

Project description:Rapid impulse propagation is a defining attribute of the pectinated atrial myocardium and His-Purkinje system (HPS) that safeguards against atrial and ventricular arrhythmias, conduction block, and myocardial dyssynchrony. The complex transcriptional circuitry that dictates rapid conduction remains incompletely understood. Here, we demonstrate that ETV1 (ER81)-dependent gene networks dictate the unique electrophysiological characteristics of atrial and His-Purkinje myocytes. Cardiomyocyte-specific deletion of ETV1 results in cardiac conduction abnormalities, decreased expression of rapid conduction genes (Nkx2-5, Gja5, and Scn5a), HPS hypoplasia, and ventricularization of the unique sodium channel properties that define Purkinje and atrial myocytes in the adult heart. Forced expression of ETV1 in postnatal ventricular myocytes (VMs) reveals that ETV1 promotes a HPS gene signature while diminishing ventricular and nodal gene networks. Remarkably, ETV1 induction in human induced pluripotent stem cell-derived cardiomyocytes increases rapid conduction gene expression and inward sodium currents, converting them towards a HPS phenotype. Our data identify a cardiomyocyte-autonomous, ETV1-dependent pathway that is responsible for specification of rapid conduction zones in the heart and demonstrate that ETV1 is sufficient to promote a HPS transcriptional and functional program upon VMs.

| S-EPMC6028599 | biostudies-literature

ETV1 knockdown in GIST cell lines

2010-10-13 | GSE19396 | GEO

Transcription factor ETV1 is essential for rapid conduction in the heart.

Project description:Rapid impulse propagation in the heart is a defining property of pectinated atrial myocardium (PAM) and the ventricular conduction system (VCS) and is essential for maintaining normal cardiac rhythm and optimal cardiac output. Conduction defects in these tissues produce a disproportionate burden of arrhythmic disease and are major predictors of mortality in heart failure patients. Despite the clinical importance, little is known about the gene regulatory network that dictates the fast conduction phenotype. Here, we have used signal transduction and transcriptional profiling screens to identify a genetic pathway that converges on the NRG1-responsive transcription factor ETV1 as a critical regulator of fast conduction physiology for PAM and VCS cardiomyocytes. Etv1 was highly expressed in murine PAM and VCS cardiomyocytes, where it regulates expression of Nkx2-5, Gja5, and Scn5a, key cardiac genes required for rapid conduction. Mice deficient in Etv1 exhibited marked cardiac conduction defects coupled with developmental abnormalities of the VCS. Loss of Etv1 resulted in a complete disruption of the normal sodium current heterogeneity that exists between atrial, VCS, and ventricular myocytes. Lastly, a phenome-wide association study identified a link between ETV1 and bundle branch block and heart block in humans. Together, these results identify ETV1 as a critical factor in determining fast conduction physiology in the heart.

| S-EPMC5127680 | biostudies-literature

Expression profiling of mouse primary prostate luminal cells from WT and T-ETV1 mice, which contains human ETV1 cDNA under the endogenous Tmprss2 promoter.

Project description:Chromosomal rearrangements involving ETS factors, ERG and ETV1, occur frequently in prostate cancer. We here examine mouse prostate cells from WT mice with s with T-ETV1 mice, which contains express the truncated human ETV1 under the endogenous Tmprss2 promoter. ETV1 expression can be tracked by GFP expression.

2013-03-01 | GSE39355 | GEO

Mapping of ETV1 genomic binding sites in gastrointestinal stromal tumor (GIST).

Project description:ETV1 is highly expressed in GIST and their presumed precursors--the interstitial cells of Cajal. ETV1 is required for survival for both GIST and ICC and regulates GIST signature genes. Here, using Illumina-Solexa based next-generation sequencing of ETV1 chromatin immunoprecipates (ChIP-Seq), we define ETV1 binding sites in the GIST48 cell line.

2010-10-14 | GSE22441 | GEO

Transcriptional effect of ETV1 knockdown in melanoma cells

Project description:ETV1 is amplified in a subset of melanomas. Here, we performed RNA-seq on two BRAF V600E mutant melonoma cell lines transduced with a scrambed shRNA and two individual ETV1 shRNA

2018-04-15 | GSE80352 | GEO

ETV1 binding sites in GIST and Melanoma cells

Project description:ETV1 is an oncogene in GIST and melanoma and a downstream transcriptional effector of MAP kinase signaling. Here, mapped the ETV1 binding sites in GIST and melanoma cell lines using ChIP-seq.

2018-04-15 | GSE80443 | GEO

ETV1 knockdown in GIST cell lines

Project description:ETV1 is highly expressed in GIST cells and required for their survival and growth. To identify genes and pathways regulated by ETV1 in GIST, we performed expression profiles of GIST cells after ETV1 knockdown. Two GIST cell lines (GIST48 and GIST882) were infected in duplicate with three shRNA viruses (Scrambled, ETV1sh1-B11TRCN0000013923, ETV1sh2-TRCN0000013925). Four days after infection, RNA was harvested for expression profiling.

2010-10-13 | E-GEOD-19396 | biostudies-arrayexpress

ETV1 and ERG genome binding/occupancy profiling by genome tiling array

Project description:Chromosomal rearrangements involving ETS factors, ERG and ETV1, occur frequently in prostate cancer. How these factors contribute to tumorigenesis and whether they play similar in vivo roles remain elusive. We show that ERG and ETV1 control a common transcriptional network but in an opposing fashion. In mice with ERG or ETV1 targeted to the endogenous Tmprss2 locus, either factors cooperated with Pten-loss, leading to localized cancer, but only ETV1 supported development of advanced adenocarcinoma, likely through enhancement of androgen receptor signaling and steroid biosynthesis. Indeed, ETV1 expression promotes autonomous testosterone production, which may contribute to tumor progression to castration-resistant prostate cancer. Patient data confirmed association of ETV1 expression with aggressive disease. We conclude that despite many shared targets, ERG and ETV1 contribute differently to prostate tumor biology. Hence, prostate cancers with these fusions should be considered as distinct subtypes for patient stratification and therapy.

2013-03-01 | GSE39357 | GEO

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