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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE28186 | GEO | 2011/03/26

SECONDARY ACCESSION(S): PRJNA139545

REPOSITORIES: GEO

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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

Genomic profiling of a RYR1-deficient skeletal muscle

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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

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

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

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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”).

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Nkx2.5 regulates Jarid2 during outflow tract morphogenesis

2010-05-17 | GSE17936 | GEO

Purkinje neurons with loss of STIM1 exhibit age-dependent changes in gene expression and synaptic components

Project description:The Stromal interaction molecule 1 (STIM1) is an ER-Ca2+ sensor and an essential component of ER-Ca2+ store operated Ca2+entry (SOCE). Loss of STIM1 affects metabotropic Glutamate Receptor 1 (mGluR1) mediated synaptic transmission, neuronal Ca2+ homeostasis and intrinsic plasticity in Purkinje Neurons (PNs). Long-term changes of intracellular Ca2+ signaling in PNs lead to neurodegenerative conditions, as evident in individuals with mutations of the ER-Ca2+ channel, the Inositol, 1,4,5-triphosphate receptor (IP3R). Moreover, Changes in gene expression upon reduced SOCE in non-excitable immune cells, the developing mouse brain, Drosophila pupal neurons and human neural precursor cells have been reported. Gene expression profiles of mature differentiated neurons with loss of STIM1/nSOC have not been published to date. The study evaluated the differential gene expression in STIM1 knockout purkinje neurons compared to wild type purkinje neurons from 1 year old mice. Analysis of gene expression profiles demonstrated that STIM1 dependent Ca2+ homeostasis and signaling helps to maintain the expression of multiple key components of synaptic architecture and function in ageing animals. Our findings are significant in the context of finding new therapeutic means of alleviating the neurodegenerative changes associated with human SCAs.

2021-03-22 | GSE158513 | GEO

Anterior Heart Field (AHF)-conditional Mef2c Knockout

Project description:We have performed conditional inactivation of mef2c in the anterior heart field (AHF) of mice and observed a phenotypic spectrum of outflow tract anomalies in the conditional mutant hearts. In an effort to identify misregulated genes in the outflow tracts of the mutants, we have performed RNA-Seq on outflow tract samples dissected from E10.5 mutant and wild-type embryos. There are four wild-type samples and four mutant samples.

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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.

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