Browse
Submit Data
Databases
API
Help

Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcription profile of hearts extracted from zebrafish embryos treated with SU5402 at 48 hpf

ABSTRACT: Heart formation requires input from two populations of progenitor cells - the first and second heart fields - that differentiate at distinct times and create different cardiac components. The cardiac outflow tract (OFT) is built through recruitment of late-differentiating, second heart field (SHF) -derived cardiomyocytes to the arterial pole of the heart. Mechanisms responsible for selection of an appropriate number of OFT cells from the SHF remain unclear, although several lines of evidence emphasize the importance of FGF signaling in promoting this process. Here, we examine the impact of inhibition of FGF signaling on cardiac transcription profiles in an effort to identify genes operating downstream of FGF during OFT development. We compared hearts from embryos treated with the FGFR inhibitor SU5402 to the hearts from sibling embryos treated with DMSO. Two replicates were performed.

ORGANISM(S): Danio rerio

SUBMITTER: Xin-Xin Zeng

PROVIDER: E-GEOD-55540 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

ACCESS DATA

Json Xml

Publications

Cadm4 restricts the production of cardiac outflow tract progenitor cells.

Zeng Xin-Xin I XX Yelon Deborah D

Cell reports 20140509 4

Heart assembly requires input from two populations of progenitor cells, the first and second heart fields (FHF and SHF), that differentiate at distinct times and create different cardiac components. The cardiac outflow tract (OFT) is built through recruitment of late-differentiating, SHF-derived cardiomyocytes to the arterial pole of the heart. The mechanisms responsible for selection of an appropriate number of OFT cells from the SHF remain unclear. Here, we find that cell adhesion molecule 4 ( ...[more]

PMID: 24813897

Similar Datasets

Transcription profile of hearts extracted from zebrafish embryos treated with SU5402 at 48 hpf

Project description:Heart formation requires input from two populations of progenitor cells - the first and second heart fields - that differentiate at distinct times and create different cardiac components. The cardiac outflow tract (OFT) is built through recruitment of late-differentiating, second heart field (SHF) -derived cardiomyocytes to the arterial pole of the heart. Mechanisms responsible for selection of an appropriate number of OFT cells from the SHF remain unclear, although several lines of evidence emphasize the importance of FGF signaling in promoting this process. Here, we examine the impact of inhibition of FGF signaling on cardiac transcription profiles in an effort to identify genes operating downstream of FGF during OFT development.

2014-05-12 | GSE55540 | GEO

Pbx4 limits vertebrate heart size and promotes pharyngeal arch artery development through partitioning progenitor fates within the second heart field and restricting proliferation

Project description:Development of the vertebrate heart requires the appropriate integration of temporally-distinct differentiating progenitor populations. While factors that promote accrual of later-differentiating second heart field (SHF)-derived cells to the outflow tract (OFT) have been intensively investigated, few signals are understood that specifically restrict the size of the vertebrate OFT. Here, we show that improper specification and proliferation of SHF progenitors in zebrafish lazarus (lzr) mutants, which lack the transcription factor Pbx4, produces enlarged hearts with a specific increase in ventricular cardiomyocytes and smooth muscle cells within the OFT. Specifically, optogenetic lineage-tracing demonstrates Pbx4 initially promotes the proper partitioning of the SHF into anterior progenitors, which contribute to the OFT, and adjacent endothelial cell progenitors, which contribute to posterior pharyngeal arch arteries. Subsequently, Pbx4 also limits the size of the SHF through repressing SHF progenitor proliferation. Single-cell RNA sequencing of nkx2.5+ cells revealed that the enlarged SHF progenitor population within Pbx4-deficient embryos assimilates characteristics of normally distinct proliferative and more anterior, differentiated cardiomyocyte populations. Therefore, the generation of proper OFT size and great arteries in vertebrates requires Pbx-dependent stratification of unique progenitor differentiation states to facilitate homeotic-like transformations and limit progenitor production within the SHF.

2020-02-19 | GSE126647 | GEO

Global gene expression changes in E9.5 cardiopharyngeal mesoderm (CPM) of Chd7 mutants versus controls

Project description:To investigate the role of Chd7 in the CPM we performed RNA-seq on two microdissections from Mesp1-Cre; Chd7 fl/fl (referred to as cKO) and control (Mesp1-Cre) embryos. The first involved the distal pharyngeal apparatus, i.e. arches two through six including the dorsal pericardial wall (DPW) which encompasses the SHF before these cells migrate to the poles of heart. For simplicity we refer to this dissection as “SHF” (we use inverted commas in this denotation to recognise the presence of other cell types). The second microdissection included the cells that have entered the heart (i.e. SHF-derived outflow tract (OFT), right ventricle (RV) and parts of the atrium, and FHF-derived left ventricle and atria). The OFT and heart tissue was collected from the same embryos (labelled “HEART”).

2023-04-29 | GSE229629 | GEO

HDAC1-mediated repression of the retinoic acid-responsive gene ripply3 promotes second heart field development

Project description:Coordinated transcriptional and epigenetic mechanisms that direct development of the later differentiating second heart field (SHF) progenitors remain largely unknown. Here, we show that a novel zebrafish histone deacetylase 1 (hdac1) mutant allele cardiac really gone (crg) has a deficit of ventricular CMs and smooth muscle within the outflow tract (OFT) due to both cell and non-cell autonomous loss in SHF progenitor proliferation. Cyp26-deficient embryos, which have increased retinoic acid (RA) levels, have similar defects in SHF-derived OFT development. We found that nkx2.5+ progenitors from hdac1 and cyp26-deficient embryos have ectopic expression of ripply3, a transcriptional co-repressor of T-box transcription factors that is normally restricted to the posterior pharyngeal endoderm. Furthermore, the ripply3 expression domain is expanded anteriorly into the posterior nkx2.5+ progenitor domain in crg mutants. Importantly, excess ripply3 is sufficient to repress VC development, while genetic depletion of Ripply3 and Tbx1 in crg mutants can partially restore VC number. We find that in crg mutants the epigenetic signature at RA response elements (RAREs) that can associate with Hdac1 and RA receptors (RARs) becomes indicative of transcriptional activation. Our study highlights that transcriptional repression via the epigenetic regulator Hdac1 facilitates OFT development through directly preventing expression of the RA-responsive gene ripply3 within SHF progenitors.

2019-05-11 | GSE126747 | GEO

Musashi-2 HITS-CLIP sequencing in K562 cells

Project description:Hematopoietic stem cells (HSCs) are maintained through the regulation of symmetric and asymmetric cell division. We report that conditional ablation of the RNA-binding protein Msi2 results in a failure of HSC maintenance and engraftment caused by a loss of quiescence and increased commitment divisions. Contrary to previous studies, we found that these phenotypes were independent of Numb. Global transcriptome profiling and RNA target analysis uncovered Msi2 interactions at multiple nodes within pathways that govern RNA translation, stem cell function, and TGF-β-signaling. Msi2-null HSCs are insensitive to TGF-β–mediated expansion and have decreased signaling output, resulting in a loss of myeloid-restricted HSCs and myeloid reconstitution. Thus, Msi2 is an important regulator of the HSC translatome and balances HSC homeostasis and lineage bias. One empty vector control– and two Flag-MSI2–overexpressing K562 cell samples were analyzed using HITS-CLIP protocol

2014-10-07 | E-GEOD-62115 | biostudies-arrayexpress

Expression in Drosophila Insensitive mutant

Project description:Affymetrix arrays measuring gene expression in 3 Drosophila Insensitive mutant embryos and 3 Drosophila wt mutant embryos 6 samples, 3 replicates of Insensitive mutants and 3 replicates of wt

2013-04-04 | E-GEOD-44177 | biostudies-arrayexpress

Single-cell transcriptomic analysis reveals lineage hierarcies and communications for second heart lineage deployment [RNA-seq]

Project description:We used single-cell RNA-seq to reconstruct differentiation paths of cardiac progenitors in two sequential waves during early heart development. Further analysis identified six major cell types and multiple differentiation trajectories of cardiac progenitors derived from distinct heart fields. We also constructed TF regulatory networks controlling SHF CPC differentiation. Interlineage crosstalk through signaling pathways and chemotactic guidance played a potent role in SHF CPC deployment. The mechanisms regulating SHF CPC migration and differentiation was further confirmed by Nkx2-5 CPC enhancer knock out. Our work provides a cardiac lineage hierarchy and new insights of SHF CPC development.

2019-06-22 | GSE108879 | GEO

Single-cell transcriptomics reveals chemotaxis mediated intra-organ crosstalk during cardiogenesis [ChIP-seq]

Project description:We used single-cell RNA-seq to reconstruct differentiation paths of cardiac progenitors in two sequential waves during early heart development. Further analysis identified six major cell types and multiple differentiation trajectories of cardiac progenitors derived from distinct heart fields. We also constructed TF regulatory networks controlling SHF CPC differentiation. Interlineage crosstalk through signaling pathways and chemotactic guidance played a potent role in SHF CPC deployment. The mechanisms regulating SHF CPC migration and differentiation was further confirmed by Nkx2-5 enhancer knock out. Our work provides a cardiac lineage hierarchy and new insights into SHF CPC development. Mechanistically, NKX2-5 directly bound the Cxcr2 genomic locus and activated its transcription.

2019-06-22 | GSE108961 | GEO

Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

Project description:The transcription factor Nkx2.5 is required for specification of pharyngeal arch second heart field (SHF) progenitors that contribute to outflow tract (OFT) and right ventricle (RV) formation. Multiple sets of microarray data were analyzed to identify genes that are candidate targets of Nkx2.5 in the second heart field. These sets are: 1) publicly available data for cardiothoracic tissue from E9.5 Nkx2.5 wild-type, heterozygous and homozygous embryos; 2) an analysis of mouse E10.5 pharyngeal arch tissue; 3) an analysis of mouse E12.5 heart tissue; and 4) a temporal analysis of the cardiogenic cell line P19CL6. This combined analysis identified 11 genes (Lrrn1, Elovl2, Safb, Slc39a6, Khdrbs1, Hoxb4, Fez1, Ccdc117, Jarid2, Nrcam, and Enpp3) expressed in SHF-containing pharyngeal arch tissue whose regulation is dependent on Nkx2.5 expression. Refer to individual Series

2010-05-17 | E-GEOD-17936 | biostudies-arrayexpress

Expression data from early and late born Atoh1 lineages within the E14.5 rhombomere 1 and isthmus

Project description:Following neural tube closure at around E9.5, the rhombic lip within the rhombomere 1/isthmus region ("upper rhombic lip") produces a sequence of neuronal lineages that populate the brainstem and cerebellum. The transcription factor Atoh1 (Math1) is required for this specialized neurogenesis, although the genetic programs that delineate the temporal cell fate changes downstream of Atoh1 are not well characterized. We examined the gene expresion changes that take place within Atoh1 lineages We purified early (E10.5) and late (E13.5) born Atoh1 expressing cells from E14.5 embryos using a transgenic labeling strategy, and analyzed differences in gene expression across the two populations using the microarray data shown below.

2011-01-01 | E-GEOD-26355 | 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