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ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification [RNA-Seq]

ABSTRACT: By RNA sequencing, we report here some hemato-vascular genes could be induced and some mesodermal/ cardiac genes could be repressed by SCL with delay in ES cell derived day 4.75 endothelial cells in the absence of ETV2

ORGANISM(S): Mus musculus

PROVIDER: GSE92535 | GEO | 2017/12/12

SECONDARY ACCESSION(S): PRJNA357999

REPOSITORIES: GEO

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ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification [ChIP-Seq]

Project description:By comparing SCL binding in day 4 Etv2KOiSCL and Etv2KOiETV2 mesodermal cells to WT, we showed delayed gene activation or repression could not be simly explained by loss of SCL binding in Etv2KOiSCL mesodermal cells

2017-12-12 | GSE92536 | GEO

ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification [ATAC-Seq]

Project description:By performing ATAC sequencing in WT, Etv2KoiSCL and Etv2KOiETV2 ES cell derived day 4.75 endothelial cells, we report here ETV2 increases chromatin accessiblity at its binding sites.

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ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification

Project description:ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification

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ETV2 cooperates with SCL for timely gene activation during hemogenic endothelium specification

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

2017-12-12 | GSE92537 | GEO

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [ChIP-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. ChIP-seq with Scl, Hand1, Lsd1, Ezh2, H3K4me1 and H3K27ac in different cell types with mesodermal origin. Scl ChIP-seq in WT, SclKO, SclKO-iScl and Gata12KO mES cell derived day4 EB (embryoid body) Flk1+ mesodermal cells, SclKO-iScl ES cells and MEL cells; Hand1 ChIP-seq in WT mES cell derived day4 EB Flk1+ mesodermal cells; Lsd1 and Ezh2 ChIP-seq in WT and SclKO mES cell derived day4 EB Flk1+ mesodermal cells. ChIP-seq of histone modifications H3K4me1 and H3K27ac in WT, SclKO and Gata12KO mES cell derived day4 EB Flk1+ mesodermal cells, HPC7 hematopoietic progenitor cells and HL1 cardiomyogenic cells

2015-01-01 | E-GEOD-47082 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [expression]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl target genes in ES cell derived day4 EB (embryoid body) Flk+ mesodermal cells

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Scl Represses Cardiomyogenesis in Prospective Hemogenic Endothelium and Endocardium

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Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [RRBS]

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Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [expression]

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Comparison of Flk-1+/Etv2- vs Flk-1+/Etv2+ populations

Project description:Screening for genes up in Etv2+ cells within Flk-1+ ES derived mesoderm Microarray analysis performed to screen for the candidate genes regulated by Etv2. Differentiated Flk-1+ mesoderm can be devided into Etv2+ or-. Etv2+ cells are assumed to be committed to hemato/endothelial cells. Comparison of two populations can reveal genes relevant in this commitment.

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