Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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”).

ORGANISM(S): Mus musculus

PROVIDER: GSE229629 | GEO | 2023/04/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression analysis of genes regulated by RBPJ (Notch) and Axin2 (Wnt) mediated signaling in mouse cardiogenesis at E9.25

Project description:Progenitor cells of the first and second heart fields (FHF and SHF) depend on cardiac-specific transcription factors for their differentiation. In mouse mutant embryos, we define the hierarchy of signaling events that controls the expression of cardiac-specific transcription factors during commitment of SHF progenitors at E9.25. Wnt and Bmp act downstream of Notch/RBPJ at this developmental stage. Mutation of Axin2, the negative regulator of canonical Wnt signaling, enhances Wnt and Bmp signals and suffices to rescue the cardiac differentiation arrest caused by loss of RBPJ. By analysis of isolated cardiac progenitors, embryo cultures in the presence of pharmacological inhibitors, and Bmp triple mutants, we could classify the expression of heart-specific transcription factors of SHF progenitors according to their dependence on either Wnt or Bmp signals, Nkx2-5, Isl1, Baf60c and Gata4, SRF, Mef2c, respectively. Total RNA from whole embryonic hearts of control mice was compared to MesP1-cre:RBPJlox/lox (KO), MesP1-cre:RBPJlox/lox//Axin2-/- (DKO), MesP1-cre:RBPJlox/+//Axin2-/- (hetDKO) and MesP1-cre:RBPJlox/lox//Axin2+/- (DKOhet) mutant mouse embryos.

2012-06-20 | E-GEOD-36804 | biostudies-arrayexpress

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

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

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

Early lineage restriction and regional segregation during mammalian heart development

Project description:Cardiac development arises from two sources of mesoderm progenitors, the first (FHF) and the second heart field (SHF). Mesp1 has been proposed to mark the most primitive multipotent cardiac progenitors common for both heart fields. Here, using clonal analysis of the earliest prospective cardiovascular progenitors in a temporally controlled manner during the early gastrulation, we found that Mesp1 progenitors consist of two temporally distinct pools of progenitors restricted to either the FHF or the SHF. FHF progenitors were unipotent, while SHF progenitors, were either uni- or bipotent. Microarray and single cell RT-PCR analysis of Mesp1 progenitors revealed the existence of molecularly distinct populations of Mesp1 progenitors, consistent with their lineage and regional contribution. Altogether, these results provide evidence that heart development arises from distinct populations of unipotent and bipotent cardiac progenitors that independently express Mesp1 at different time points during their specification, revealing that the regional segregation and lineage restriction of cardiac progenitors occurs very early during gastrulation. We used microarrays to characterize the molecular mechanisms that control Mesp1 progenitor specification and lineage segregation during the early stage of cardiac mesoderm formation, 50 Mesp1 H2B-GFP+ or Mesp1 H2B-GFP- cells at E6.5 or E7.5 from mouse embryos were sorted for RNA extraction, amplification and hybridization on Affimetrix microarrays. Microaarrays were performed on Mouse Genome 430 PM strip Affymetrix array. The overall design was repeated in two different biological samples.

2014-07-10 | E-GEOD-59033 | biostudies-arrayexpress

Early lineage restriction and regional segregation during mammalian heart development

2014-07-10 | GSE59033 | GEO

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

2014-05-12 | E-GEOD-55540 | biostudies-arrayexpress

Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

2010-05-17 | GSE17936 | GEO

HIC2 regulates maturation of the cardiovascular system

Project description:HIC2 is required for normal development of the heart. Loss of function mutants exhibit early embryonic lethality while heterozygous mutants have a partially penetrant ventricular septal defect. The aim of this study was to understand the function of HIC2 in early heart development by identifying potential transcriptional targets. We harvested whole hearts (which contain circulating erythrocytes) at embryonic day E9.5 and compared expression in a conditional loss of function mutant (Mesp1 Cre/+; Hic2 Fl/Fl) to controls (Hic2 Fl/Fl).

2017-06-17 | GSE100125 | 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

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