Mouse Embryonic 12.5 mouse heart transcriptome
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE64147 | GEO | 2018/12/01
REPOSITORIES: GEO
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Project description:We prepared RNA from mouse embryonic hearts and performed mRNA micro-array analysis to compare gene expression profiles between control and Rhau-deletion mice (E12.5), in order to understand how RHAU regulates heart development.
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Project description:This study was conducted to examine normal gene expression in the heart during mouse embryonic development. Wild type embryo hearts (n=5) were collected at stage E12.5 and total RNA was isolated for analysis by Affymetrix mouse genome 430A GeneChip.
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Project description:Purpose: The goals of this study are to characterize and analyze the emrbyonic heart transcriptome profiling (RNA-seq) at E9.5, E10.5, E12.5, E14.5 and E16.5. Methods: mRNA profiles of E9.5, E10.5, E12.5, E14.5 and E16.5 C57/Bl6 mouse embryonic hearts were generated by deep sequencing, n=3 or 4 for each age, using Illumina HiSeq2500. Results: Using an optimized data analysis workflow, we mapped at least 36 million sequence reads per sample to the mouse genome (build mm10) and identified 17,537 transcripts in the mouse hearts.
2023-04-07 | GSE223237 | GEO
Project description:Mice lacking the zinc finger transcription factor Specificity protein 3 (Sp3) die prenatally in the C57Bl/6 background. To elucidate the cause of mortality we analyzed the potential role of Sp3 in embryonic heart development. Sp3 null hearts display defective looping at E10.5, and at E14.5 the Sp3 null mutants have developed a range of severe cardiac malformations. In an attempt to position Sp3 in the cardiac developmental hierarchy, we analysed the expression patterns of >15 marker genes in Sp3 null hearts. Expression of Cardiac ankyrin repeat protein (Carp) was downregulated prematurely after E12.5, while expression of the other marker genes was not affected. ChIP analysis revealed that Sp3 is bound to the Carp promoter region in vivo. Microarray analysis indicates that small molecule metabolism and cell-cell interactions are the most significantly affected biological processes in E12.5 Sp3 null myocardium. Since the epicardium showed distension from the myocardium, we studied expression of Wt1, a marker for epicardial cells. Wt1 expression was diminished in epicardium-derived cells in the myocardium of Sp3 null hearts. We conclude that Sp3 is required for normal cardiac development, and suggest that it has a crucial role in myocardial differentiation. ( Experiment Overall Design: Hearts were dissected from E12.5 wildtype (n=3) and Sp3 knockout (n=3) fetuses. Total RNA was isolated from individual hearts; 5μg was used for labelling and hybridization to 430 2.0 Gene Chips (a total of 6).
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Project description:The Dp1Tyb mouse model for Down syndrome contains a duplication of 23Mb of mouse chromosome 16 (Mmu16) that is orthologous to human chromosome 21 (Hsa21). This region contains 145 coding genes, and thus these genes are present in 3 copies. Dp1Tyb mice display congenital heart defects, similar to the ones seen in people with Down syndrome. These defects include ventricular and atrio-ventricular septal defects and are seen at embryonic day 14.5 (E14.5) of gestation. One of the 145 genes present in 3 copies in Dp1Tyb mice codes for a kinase called DYRK1A. We found that by crossing Dp1Tyb mice with mice carrying a heterozygous Dyrk1a loss of function allele, thereby reducing the dosage of the Dyrk1a gene from 3 to 2 copies, we rescue the congenital heart defects. Thus 3 copies of Dyrk1a are required to cause heart defects, and, presumably, increased DYRK1A protein is required for the heart defects. We compared the phosphoproteome in Dp1Tyb versus Dp1TybDyrk1a+/+/- embryonic hearts in order to discover alterations in phosphoproteins that could pinpoint molecular mechanisms that give rise to the congenital heart defects. The two strains (Dp1Tyb and Dp1TybDyrk1a+/+/-) differ only in the copy number of Dyrk1a (3 v 2) and thus differences in phosphoproteins would include both direct and indirect targets of DYRK1A activity.
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Project description:We generated mouse heart organoids from mouse embryonic stem cells. The heart organoids showed both atrium-like and ventricle-like morphology similar to those of embryonic hearts. Therefore we performed RNA-seq analysis to compare atrial and ventricular gene expression profiles between mouse embryonic hearts and induced heart organoids.
2020-06-30 | GSE143932 | GEO
Project description:In order to identify the targets of GATA4-FOG2 action in mammalian heart development we performed Affymetrix microarray comparisons of gene expression in normal and mutant at embryonic (E) day E12.5 hearts. We compared RNA samples from both Fog2-null and Gata4ki/ki mutant E12.5 hearts to the wild-type control E12.5 hearts. We reasoned that as the phenotypes of the Fog2 knockout and Gata4ki/ki mutation (a V217G mutation that specifically cripples the interaction between GATA4 and FOG proteins) are similar, we should expect to identify a similar set of differentially expressed genes in both experiments. As an additional control, we expected to find the Fog2 gene expression absent in the mutant (null) Fog2 cardiac sample, but not Gata4ki/ki sample. We have analyzed 6 RNA samples total (3 from control hearts, 2 from FOG2 null hearts and 1 from GATA4ki hearts)
2010-02-21 | E-GEOD-14906 | biostudies-arrayexpress
Project description:Purpose: The goals of this study are to compare transcriptome profiling (RNA-seq) resulting from a Mesp1Cre driven ablation of Hira in the heart at E11.5 and E12.5. Methods: RNA extraction was done in triplicate from Mesp1Cre;Hira-/fl and Mesp1Cre;Hira+/fl embryonic hearts at E11.5 and E12.5 using the QIAGEN RNeasy mini kit. RNAseq was processed by the ICH genomics facility, reads were aligned and normalised using BOWTIE and DEseq R package. Strand NGS 2.5 software was used to re-analyse the aligned files (.bam). By applying the Mann Whitney unpaired test, Benjamini Hochberg False discovery rate (FDR) and filtering the genes using adjusted p-value ≤ 0.05 and absolute fold change ≥ 1.5, 95 % of the results were identical to the DEseq package used by the UCL Genomics facility. Results: We identified 360 coding transcripts changed in the mutant hearts (Mann Whitney unpaired test, Benjamini Hochberg FDR, p ≤ 0.05, FC ≥ 1.5) with no trend towards up- or down-regulation of global transcription (48.8% down vs 51.2% up) at E12.5. Conclusions: This work analyses the role of HIRA in mouse cardiac development. It was found that Tnni2 is the most upregulated gene in the absence of Hira. qRT-PCR validation of 25 targets. Little (<5%) or no variation of fold change between RNAseq and qRT-PCR data were observed.
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Project description:Ischemia reperfusion (I/R) injury is an unavoidable event occurring during heart transplantation, leading to graft failures and lower long-term survival rate of the recipient. microRNAs are major regulators of genes. IR causes apoptosis/death of cardiomyocytes, resulting from up-regulation of apoptotic genes and down-regulation of anti-apoptotic genes which are regulated by microRNA. We used microarrays to detail the global programme of gene expression underlying cellularisation and identified distinct classes of up-regulated genes during this process. We perserved donor hearts with university of Wisconsin solution for 18h at 4C degree before being implanted into recipients to create ischemia reperfusion injury. The preserved hearts were implanted into a syngeneic recipient mice. 24h after transplantation, heart grafts were harvested for microRNA extraction.
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