Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Endothelial progenitor migration and differentiation is regulated by distinct transcriptional effectors of Cloche/Npas4l

ABSTRACT: Embryonic cells including endothelial progenitors undergo extensive migration and differentiation events; however, whether and how these processes are interrelated remains unclear. The transcription factor Npas4l is necessary for endothelial specification in zebrafish by inducing the expression of the transcription factor genes etsrp, tal1 and lmo2. We generated a knock-in reporter in the npas4l locus to visualize endothelial progenitors and their derivatives in wild-type and mutant embryos. We find that in npas4l mutants, npas4l reporter expressing cells do not migrate to the midline and instead contribute to skeletal muscle and pronephric tubules. Investigating the Npas4l transcriptional effectors, we find that npas4l reporter expressing cells in tal1 mutants fail to migrate while those in etsrp mutants migrate but fail to differentiate. In lmo2 mutants, npas4l reporter expressing cells migrate and differentiate, but many express pronephric tubule markers. Altogether, these data reveal the complex regulation of endothelial progenitor migration, differentiation and fate restriction.

ORGANISM(S): Danio rerio

PROVIDER: GSE166396 | GEO | 2022/07/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Genome-wide strategies reveal downstream target genes of Npas4l associated with vascular development in zebrafish [ChIP-Seq]

Project description:The development of a vascular network is essential to nourish tissues and sustain organ function throughout life. Endothelial cells (ECs) are the building blocks of blood vessels, yet our understanding of EC specification in vertebrates remains incomplete. cloche/npas4l mutants have broadly been used as an avascular model in zebrafish, but little is known about the molecular mechanism of action of Npas4l. Here, to identify the direct and indirect target genes of this transcription factor, we combined complementary genome-wide approaches, including transcriptome analyses and chromatin immunoprecipitation (ChIP). The cross-analysis of these datasets indicate that Npas4l functions as a master regulator by directly inducing a wave of transcription factor genes crucial for hematoendothelial specification in vertebrates, including etv2, tal1, and lmo2. We identified additional target genes acting downstream of npas4l and investigated the function of a subset of them using CRISPR/Cas9 technology. Phenotypic characterization of tspan18b mutants reveals a novel role for tspan18b in developmental angiogenesis, confirming the reliability of the datasets generated. Collectively, these data represent a useful resource for future studies aimed to investigate novel genes with a potential role in vascular development and EC fate determination in vertebrates.

2019-05-21 | GSE130198 | GEO

Genome-wide strategies reveal downstream target genes of Npas4l associated with cardiovascular development in zebrafish [RNA-Seq 2]

2019-05-21 | GSE130200 | GEO

Genome-wide strategies reveal downstream target genes of Npas4l associated with cardiovascular development in zebrafish [RNA-Seq 1]

2019-05-21 | GSE130199 | GEO

Genome-wide strategies reveal downstream target genes of Npas4l associated with cardiovascular development in zebrafish [ATAC-Seq]

2019-05-21 | GSE130196 | GEO

Microarray analysis of the Endo and eVSM populations for the A2lox.i8TFs cell line

Project description:The aim of the experiment was to study the transcriptome changes occuring after overexpression of Erg, Fli1, Tal1, Lyl1, Lmo2, Runx1, Cbfb and Gata2 in endothelial (Endo) and enriched vascular smooth muscles (eVSM) populations.

2018-03-20 | GSE96836 | GEO

LMO2 Is Required for TAL1 DNA Binding Activity and Initiation of Definitive Haematopoiesis at the Haemangioblast Stage

Project description:We differentiated WT, LMO2KO or TAL1 KO mouse ES cell lines into Flk-1+ haemangioblasts and/or Tie2+;Kit+;CD41- haemogenic endothelium 1 (HE1). We performed RNAseq, ChIPseq and/or DHS seq on these cells and compared the samples. Our study showed that Lmo2-/- embryonic stem cells differentiated less efficiently to haemogenic endothelium, which only produced primitive haematopoietic progenitors. LMO2 was required at the haemangioblast stage to position the TAL1/LMO2/LDB1 complex to regulatory elements that are important for the establishment of the haematopoietic developmental program. In the absence of LMO2, TAL1 protein levels were low and the target site recognition of TAL1 was impaired.

2017-11-01 | GSE99938 | GEO

Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma

Project description:LMO2 regulates gene expression facilitating the formation of multipartite DNA-binding complexes. In B cells, LMO2 is specifically up-regulated in the Germinal Center (GC) reaction and is expressed in GC-derived non-Hodgkin’s lymphomas. LMO2 is one of the most powerful prognostic indicators in DLBCL patients. However, its function in GC B cells and DLBCL is currently unknown. In the present study we characterized the LMO2 transcriptome and interactome in DLBCL cells. LMO2 regulates genes implicated in kinetochore function, chromosome assembly and mitosis. Overexpression of LMO2 in DLBCL cell lines results in centrosome amplification. In DLBCL, the LMO2 complex contains some of the traditional partners such as LDB1, E2A, HEB, Lyl1, ETO2 and SP1, but not TAL1 or GATA proteins. Furthermore, we identified novel LMO2 interacting partners: ELK1, NFATc1 and LEF-1 proteins. Reporter assays revealed that LMO2 increases transcriptional activity of NFATc1 and decreases transcriptional activity of LEF-1 proteins. Overall, our studies identified a novel LMO2 transcriptome and interactome in DLBCL and provide a platform for future elucidation of LMO2 function in GC B-cells and DLBCL pathogenesis. RCK8 DLBCL cell lines were stably transfected with control plasmid or plasmid+LMO2

2012-07-12 | E-GEOD-34576 | biostudies-arrayexpress

RNA-seq of mouse Embryonic Stem Cell (mESC) line-derived endothelial and hematopoietic cells subjected to differential doxycycline (dox)-induced expression of transcription factors (TFs) in a Tal1Δ/Δ genetic background

Project description:RNA-seq of endothelial (Endo), Pre-hematopoietic progenitor cells (Pre-HPCs) and hematopoietic progenitors (HP) derived from the in-vitro hematopoietic differentiation of mouse Embryonic Stem Cells (mESCs) harboring a biallelic inactivating deletion of the endogenous Tal1 gene, and a construct for the dox-induced expression of the hematopoietic genes Tal1, Lyl1 and Lmo2 (i3TFs Tal1Δ/Δ mESCs). i: inducible. TFs: transcription factors. Cells were treated with dox at one (Dox Unt) or two (Dox Dox) time-points during hematopoietic differentiation to inducibly express the 3TFs. Sequenced cell populations were purified by FACS sorting based on the cell-surface expression of the endothelial marker VE-CADHERIN and the hematopoietic marker CD41. Endo: VE-CADHERIN+CD41- Pre-HPCs: VE-CADHERIN+CD41+ HP: VE-CADHERIN-CD41+

2023-05-15 | E-MTAB-12973 | biostudies-arrayexpress

Identification of LMO2 transcriptome and interactome in diffuse large B-cell lymphoma

2012-07-13 | GSE34576 | GEO

Genome wide RNA-sequencing of human pluripotent stem-cell derived endothelial cells 48h after transduction with adenoviruses expressing either empty vector or single transcription factor

Project description:To induce barrier of stem-cell derived endothelial cells in vitro cells have been transduced with adenoviruses overexpressing transcription factors with potential role in endothelial cell barrier stabilization. Adenoviruses overexpressing either ETS1 or FOXC1 or FOXF2 or KLF11 or SOX18 or SOX7 or TAL1 or LEF1 or LMO2 have been been used at 80 MOI. As control adenovirus overexpressing empty vectors has been used (80 MOI).

2020-03-05 | GSE142130 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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