Mouse Embryonic 12.5 mouse heart transcriptome
Ontology highlight
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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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:Lmx1b is a homeodomain transcription factor responsible for limb dorsalization. Despite striking double-ventral (loss-of-function) and double-dorsal (gain-of-function) limb phenotypes, no direct downstream gene targets in the limb have been confirmed. To determine direct targets of Lmx1b during limb dorsalization (E12.5), we performed chromatin immunoprecipitation followed by next generation sequencing (ChIP-seq). Nearly 84% (n=617) of the Lmx1b-bound genomic fragments or intervals (LBIs) identified by two Lmx1b-ChIP-seqs overlap with chromatin regulatory marks indicative of potential cis-regulatory modules (PCRMs). In addition, 73 LBIs mapped to known cis-regulatory modules (CRMs) active during limb development. We compared Lmx1b-bound PCRMs to genes differentially expressed by Lmx1b at E12.5 and found 292 PCRMs within 1 Mb of 254 Lmx1b-regulated genes. Gene ontology analysis of these associated genes suggests that Lmx1b mediates dorsalization through the regulation of extracellular matrix production, bone/joint formation, axonal guidance, vascular development, cell proliferation and cell movement. We validated the functional activity of 2 PCRMs associated to Lmx1b-regulated genes, demonstrating activity and overlap with the associated gene during limb development. This is the first report to describe the genome-wide distribution of Lmx1b binding during limb development, directly linking Lmx1b to targets that accomplish limb dorsalization.
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Project description:Transcriptional profiling of the atrioventricular canal from e10.5 mouse hearts comparing wild-type control with Tbx3 GH/N hypomorphic mutant microdissected tissue. The goal was to identify direct and indirect targets of the transcription factor Tbx3, because Tbx3 is expressed in the AVC and hypomorphs develop embryonic AV conduction block at e12.5.
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Project description:Transcriptional profiling of the atrioventricular canal from e10.5 mouse hearts comparing wild-type control with Tbx3 GH/N hypomorphic mutant microdissected tissue. The goal was to identify direct and indirect targets of the transcription factor Tbx3, because Tbx3 is expressed in the AVC and hypomorphs develop embryonic AV conduction block at e12.5. Two-condition experiment, wild-type control and Tbx3 mutant AVC tissue. Tissue from 5 hearts was pooled to make each sample. Biological replicates: 4.
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Project description:Laser capture microdissection mass spectrometry analysis on mouse embryonic tail tendon bundles, E12.5-E14.5 in half day steps.
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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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