Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [ChIP-Seq]

ABSTRACT: Embryonic blood cell development occurs via well-defined developmental stages which are recapitulated in vitro by differentiation of embryonic stem cells. This process is tightly regulated by the interaction of tissue- specific and ubiquitous transcription factors with the chromatin landscape in response to outside signals. We previously identified binding motifs for the commonly expressed AP-1 transcription factor family in open chromatin regions specific for early stages of blood specification and thus aimed to study the role of AP-1 for hemangioblast differentiation. Here we show that FOS and JUN together bind to and activate a core set of vascular genes in the hemogenic endothelium and that upon global inhibition of AP-1 by expression of a dominant negative FOS peptide the balance between endothelial and hematopoietic fate is shifted towards blood. Moreover, we demonstrate that in the hemogenic endothelium AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signaling, to vascular genes. Notably, after the endothelial-to-hematopoietic transition TEAD4 binding is no longer persisting. These findings provide novel mechanistic insights into vascular and hematopoietic development.

ORGANISM(S): Mus musculus

PROVIDER: GSE79320 | GEO | 2016/10/21

SECONDARY ACCESSION(S): PRJNA315457

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [expression]

Project description:Embryonic blood cell development occurs via well-defined developmental stages which are recapitulated in vitro by differentiation of embryonic stem cells. This process is tightly regulated by the interaction of tissue- specific and ubiquitous transcription factors with the chromatin landscape in response to outside signals. We previously identified binding motifs for the commonly expressed AP-1 transcription factor family in open chromatin regions specific for early stages of blood specification and thus aimed to study the role of AP-1 for hemangioblast differentiation. Here we show that FOS and JUN together bind to and activate a core set of vascular genes in the hemogenic endothelium and that upon global inhibition of AP-1 by expression of a dominant negative FOS peptide the balance between endothelial and hematopoietic fate is shifted towards blood. Moreover, we demonstrate that in the hemogenic endothelium AP-1 is required for de novo binding of TEAD4, a transcription factor connected to Hippo signaling, to vascular genes. Notably, after the endothelial-to-hematopoietic transition TEAD4 binding is no longer persisting. These findings provide novel mechanistic insights into vascular and hematopoietic development.

2016-10-21 | GSE79322 | GEO

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [DNase-Seq]

2016-10-21 | GSE79321 | GEO

Mesp1 induces a subset of hematopoietic-associated transcription factors in ES cell-derived Flk1+Tie2+ endothelium

Project description:Previously, we reported that the transcription factor Mesp1 promotes the cell fates of cardiomyocytes, smooth muscle, and vascular endothelium. Recently, hematopoietic stem cells (HSCs) were shown to derive from hemogenic endothelium. Since Mesp1 regulates development of endothelium, it potentially could influence gene expression related to hematopoietic development. Our present fate mapping study found that Mesp1-cre efficiently labeled hematopoietic lineages in vivo. This result suggested that Mesp1 might be expressed in progenitors of the hematopoietic system, such as hemogenic endothelium. To test this, we purified Flk1+ Tie2+ endothelium derived from differentiating ES cells with or without Mesp1 induction, and used microarray expression analysis to identify genes strongly up-regulated by Mesp1.

2012-08-03 | GSE34537 | GEO

Mesp1 induces a subset of hematopoietic-associated transcription factors in ES cell-derived Flk1+Tie2+ endothelium

2012-08-02 | E-GEOD-34537 | biostudies-arrayexpress

Hemogenic Endothelium transcriptome along the timeline of hESC differentiation

Project description:The differentiation of human embryonic stem cells to hematopoietic lineages initiates with the specification of hemogenic endothelium, a transient specialized endothelial precursor of all blood cells.Unfortunately, absence of hemogenic endothelium-specific markers as well as lack of consensus in the timing of hemogenic potential analysis and methodologies used to study the hematopoietic potential of this precursor prevents reaching clear and definite conclusions. Here, we demonstrate that the hemogenic potential of the endothelium precursor population sharply decline over the course of the differentiation process. Poly(A) RNA-sequencing on CD31+CD144+ population at day 6, day 8 and day 10 of EB diffferentiation with or without the addition of cytokines. Comparasion with hematopoietic committed population CD31+CD144- from day 10 of EB differentiation.

2018-10-25 | GSE109648 | GEO

RNA-seq to assess the impact of circulation on hematopoietic stem cell differentiation.

Project description:Blood flow promotes hematopoiesis, Definitive hematopoietic stem cells can not be assessed in circulation negative Ncx-/- mice. This study looks at the impact of lack of blood flow on the earliest blood cell precursors, the pro-HSCs. E9.5 was chosen as this is the time point pro-HSCs are normally generated. Cells from the hemogenic endothelium, the endothelium and pro-HSCs were sequenced.

2021-10-01 | E-MTAB-8362 | biostudies-arrayexpress

RUNX1 and the endothelial origin of blood

Project description:The transcription factor RUNX1 is required in the embryo for formation of the adult hematopoietic system. Here we describe the seminal findings that led to the discovery of RUNX1 and of its critical role in blood cell formation in the embryo from hemogenic endothelium. We also present RNA-Seq data demonstrating that hemogenic endothelial cells in different anatomic sites, which produce hematopoietic progenitors with dissimilar differentiation potentials, are molecularly distinct. Hemogenic endothelial cells and non-hemogenic endothelial cells in the yolk sac are more closely related to each other than either are to hemogenic or non-hemogenic endothelial cells in the major arteries. Thus, a major driver of the different lineage potentials of the committed erythro-myeloid progenitors that emerge in the yolk sac, versus hematopoietic stem cells that originate in the major arteries, is likely to be the distinct molecular properties of the hemogenic endothelial cells from which they are derived. We use bioinformatics analyses to predict signaling pathways active in arterial hemogenic endothelium, several of which are functionally validated pathways including Notch, Wnt, and Hedgehog. We also use a novel bioinformatics approach to assemble transcriptional regulatory networks and predict transcription factors that may be specifically involved in hematopoietic cell formation from arterial hemogenic endothelium, which is the origin of the adult hematopoietic system.

2018-10-05 | GSE103813 | GEO

AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification

Project description:AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification

| PRJNA315459 | ENA

Single-cell RNA-seq (10x Chromium) of FACS-sorted drl:H2B-Dendra2, etv2:Kaede, fli1:DsRed, and tp1:eGFP transgenic zebrafish embryos

Project description:Development of the dorsal aorta is a key step in the establishment of the adult blood-forming system, since hematopoietic stem and progenitor cells (HSPCs) arise from ventral aortic endothelium in all vertebrate animals studied. Work in zebrafish has demonstrated that arterial and venous endothelial precursors arise from distinct subsets of lateral plate mesoderm. Here, we profile the transcriptome of the earliest detectable endothelial cells (ECs) during zebrafish embryogenesis to demonstrate that tissue-specific EC programs initiate much earlier than previously appreciated, by the end of gastrulation. Classic studies in the chick embryo showed that paraxial mesoderm generates a subset of somite-derived endothelial cells (SDECs) that incorporate into the dorsal aorta to replace HSPCs as they exit the aorta and enter circulation. We describe a conserved program in the zebrafish, where a rare population of endothelial precursors delaminates from the dermomyotome to incorporate exclusively into the developing dorsal aorta. Whereas SDECs lack hematopoietic potential, they act as a local niche to support the emergence of HSPCs from neighboring hemogenic endothelium. Thus, at least three subsets of ECs contribute to the developing dorsal aorta: vascular ECs, hemogenic ECs, and SDECs. Taken together, our findings indicate that the distinct spatial origins of endothelial precursors dictate different cellular potentials within the developing dorsal aorta.

2023-08-01 | E-MTAB-13196 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [RNA-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. Examination of Scl and Gata 1 & 2 target genes in ES cell derived day4.75 EB (embryoid body) Tie2+CD31+CD41- endothelial cells

2015-01-01 | E-GEOD-47083 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data