AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification
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ABSTRACT:
PROVIDER: PRJNA315459 | ENA |
REPOSITORIES: ENA
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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
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 | GSE79321 | GEO
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 | GSE79320 | GEO
Project description:AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [expression]
| PRJNA315462 | ENA
Project description:AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [ChIP-Seq]
| PRJNA315457 | ENA
Project description:AP-1 and TEAD4 co-operatively promote the vascular program during hemangioblast specification [DNase-Seq]
| PRJNA315456 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2016-10-21 | GSE79323 | GEO
Project description:In the preimplantation mouse embryo TEAD4 is critical to establishing the trophectoderm (TE)-specific transcriptional program and segregating TE from the inner cell mass (ICM). However, TEAD4 is expressed both in the TE and the ICM. Thus, differential function of TEAD4 rather than expression itself regulates specification of the first two cell lineages. We used ChIP-seq to define genome-wide TEAD4 target genes and asked how transcription of TEAD4 target genes is specifically maintained in the TE. Our analyses revealed an evolutionarily conserved mechanism, in which lack of nuclear localization of TEAD4 impairs the TE-specific transcriptional program in inner blastomeres, thereby allowing their maturation towards the ICM lineage. Restoration of TEAD4 nuclear localization maintains the TE-specific transcriptional program in the inner blastomeres and prevents segregation of the TE and ICM lineages and blastocyst formation. We propose that altered subcellular localization of TEAD4 in blastomeres dictates first mammalian cell fate specification. ChIPseq profiles of TEAD4, IgG, Input in Mouse trophoblast stem cells using Illumina HiSeq 2000 and Illumina Genome Analyzer IIx
2012-04-18 | E-GEOD-37350 | biostudies-arrayexpress
Project description:In the preimplantation mouse embryo TEAD4 is critical to establishing the trophectoderm (TE)-specific transcriptional program and segregating TE from the inner cell mass (ICM). However, TEAD4 is expressed both in the TE and the ICM. Thus, differential function of TEAD4 rather than expression itself regulates specification of the first two cell lineages. We used ChIP-seq to define genome-wide TEAD4 target genes and asked how transcription of TEAD4 target genes is specifically maintained in the TE. Our analyses revealed an evolutionarily conserved mechanism, in which lack of nuclear localization of TEAD4 impairs the TE-specific transcriptional program in inner blastomeres, thereby allowing their maturation towards the ICM lineage. Restoration of TEAD4 nuclear localization maintains the TE-specific transcriptional program in the inner blastomeres and prevents segregation of the TE and ICM lineages and blastocyst formation. We propose that altered subcellular localization of TEAD4 in blastomeres dictates first mammalian cell fate specification.
2012-04-18 | GSE37350 | GEO