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Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

ABSTRACT: 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. This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE17936 | GEO | 2010/05/17

SECONDARY ACCESSION(S): PRJNA119873

REPOSITORIES: GEO

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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

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

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

Precardiac Organoids Form Two Heart Fields via Bmp/Wnt Signaling

Project description:The discovery of the first heart field (FHF) and the second heart field (SHF) led us to understand how cardiac lineages and structures arise during development. However, it remains unknown how they are specified. Here, we generate precardiac spheroids with pluripotent stem cells (PSCs) harboring GFP/RFP reporters under the control of FHF/SHF markers, respectively. GFP+ cells and RFP+ cells appear from two distinct areas and develop in a complementary fashion. Transcriptome analysis shows a high degree of similarities with embryonic FHF/SHF cells. Bmp and Wnt are among the most differentially regulated pathways, and gain- and loss-of-function studies reveal that Bmp specifies GFP+ cells and RFP+ cells via the Bmp/Smad pathway and Wnt signaling, respectively. FHF/SHF cells can be isolated without reporters by the surface protein Cxcr4. This study provides novel insights into understanding the specification of two cardiac origins, which can be leveraged for PSC-based modeling of heart field/chamber-specific disease.

2018-06-23 | GSE116128 | GEO

Analysis of gene expression in the mouse embryo pharyngeal arch

Project description:This study was conducted to examine normal gene expression in the pharyngeal arch during mouse embryonic development Wild type embryonic tissue containing the pharyngeal arches was collected from five independent samples (n=5) at stage E10.5 by dissection. Total RNA was isolated for analysis by Affymetrix mouse genome 430A GeneChip.

2010-07-07 | E-GEOD-17934 | biostudies-arrayexpress

Expression data from from the E9.25 hearts of mouse embryos

Project description:Congenital heart defects (CHDs) occur in 0.5–1% of live births, yet the underlying genetic etiology remains mostly unknown. Recently, a new source of myocardial cells, namely the second heart field (SHF), was discovered in the splanchnic mesoderm. Abnormal development of the SHF leads to a spectrum of outflow tract defects, such as persistent truncus arteriosus and tetralogy of Fallot. Intracellular Ca2+ signaling is known to be essential formany aspects of heart biology including heart development, but its role in the SHF is uncertain. Here, we analyzed mice deficient for genes encoding inositol 1,4,5-trisphosphate receptors (IP3Rs), which are intracellular Ca2+ release channels on the endo/sarcoplasmic reticulum that mediate Ca2+ mobilization. Mouse embryos that are double mutant for IP3R type 1 and type 3 (IP3R1−/−IP3R3−/−) show hypoplasia of the outflow tract and the right ventricle, reduced expression of specific molecular markers and enhanced apoptosis ofmesodermal cells in the SHF. Gene expression analyses suggest that IP3R-mediated Ca2+ signalingmay involve, at least in part, theMef2C–Smyd1 pathway, a transcriptional cascade essential for the SHF. These data reveal that IP3R type 1 and type 3 may play a redundant role in the development of the SHF. In total 4 samples were analyzed, they represent two different genotypes (wt, double ko) that were tested in duplicate each.

2011-03-26 | E-GEOD-28186 | biostudies-arrayexpress

Expression data from from the E9.25 hearts of mouse embryos

2011-03-26 | GSE28186 | GEO

scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scRNA-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

2022-07-27 | GSE198562 | GEO

scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO)

Project description:We performed scATAC-seq over multiple time points of heart development in WT C57Bl6/J embryos and in Tbx1 mutant mice (Tbx1 KO). We dissected primarily the cardiac region but also the regions dorsal to the heart and the pharyngeal arches to capture the progenitor cells that migrate into the heart and the neural crest cells. For time points E10.5 and E11.5, we primarily dissected the regions behind the heart and included less of the overall cardiac region. We included pharyngeal arches for all time points and, at E11.5, we excluded the first arch. For Tbx1 null embryos, we also generated scRNA-seq data for WT and mutant embryos from the same pool of dissociated cells used for scATAC-seq.

2022-07-27 | GSE198561 | GEO

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