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Expression data from Mus musculus Myc-null heart at E13.5

ABSTRACT: We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Keywords: wildtype vs Myc-null

ORGANISM(S): Mus musculus

PROVIDER: GSE7162 | GEO | 2007/06/30

SECONDARY ACCESSION(S): PRJNA98167

REPOSITORIES: GEO

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Expression data from Mus musculus Myc-null heart at E13.5

Project description:We created mice, which are deficient for Myc specifically in cardiac myocytes by crossing crossed Myc-floxed mice (Mycfl/fl) and MLC-2VCre/+ mice. Serial analysis of earlier stages of gestation revealed that Myc-deficient mice died prematurely at E13.5-14.5. Morphological analyses of E13.5 Myc-null embryos showed normal ventricular size and structure; however, decreased cardiac myocyte proliferation and increased apoptosis was observed. BrdU incorporation rates were also decreased significantly in Myc-null myocardium. Myc-null mice displayed a 3.67-fold increase in apoptotic cardiomyocytes by TUNEL assay. We examined global gene expression using oligonucleotide microarrays. Numerous genes involved in mitochondrial death pathways were dysregulated including Bnip3L and Birc2. Hearts were taken from wide type and Myc-null Mouse embryos at E13.5 under the dissecting scope. Cardiac myocyte RNA was isolated using TRIZOLÂ®Reagent Total RNA (100 ng) was hybridized to the SentrixÂ® MouseRef-8 Expression BeadChip that contains probes for ~24,000 transcripts. GeneChips were scanned using the Hewlett-Packard GeneArray Scanner G2500A. The data were analyzed with Illumina Inc. BeadStudio version 1.5.0.34 and normalized by rank invariant method.

2010-06-10 | E-GEOD-7162 | biostudies-arrayexpress

Mus musculus

Project description:Expression data from Mus musculus Myc-null heart at E13.5

| PRJNA98167 | ENA

Microarray skeletal muscle PGC-1alpha-/- - beta f/f/Mlc1fCre mice

Project description:Title: Total Skeletal Muscle PGC-1 Deficiency Uncouples Mitochondrial Derangements from Fiber Type Determination and Insulin Sensitivity Abstract: Evidence is emerging that the PGC-1 coactivators serve a critical role in skeletal muscle metabolism, function, and disease. Mice with total PGC-1 deficiency in skeletal muscle (PGC-1α-/- βf/f/MLC-Cre mice) were generated and characterized. PGC-1α-/-βf/f/MLC-Cre mice exhibit a dramatic reduction in exercise performance compared to single PGC-1α- or PGC-1β-deficient mice and wild-type controls. The exercise phenotype of the PGC-1α-/-βf/f/MLC-Cre mice was associated with a marked diminution in muscle oxidative capacity and mitochondrial structural derangements consistent with fusion/fission and biogenic defects together with rapid depletion of muscle glycogen stores during exercise. Surprisingly, the skeletal muscle fiber type profile of the PGC-1α-/-βf/f/MLCCre mice was not significantly different than the wild-type mice. Moreover, insulin sensitivity and glucose tolerance were also not altered in the PGC-1α-/-βf/f/MLC-Cre mice. Taken together, we conclude that PGC-1 coactivators are necessary for the oxidative and mitochondrial programs of skeletal muscle but are dispensable for fundamental fiber type determination and insulin sensitivity.

2010-12-01 | GSE23365 | GEO

Mice Lacking a Myc Enhancer Element that Includes Human SNP rs6983267 Are Resistant to Intestinal Tumors

Project description:Multiple cancer-associated single nucleotide polymorphisms (SNPs) have been mapped to conserved sequences within a 500 kilobase region upstream of the MYC oncogene on human chromosome 8q24. These SNPs may affect cancer development through altered regulation of MYC expression, but this hypothesis has been difficult to confirm. We generated mice deficient in Myc-335, a putative MYC regulatory element that contains rs6983267, a SNP accounting for more human cancer- related morbidity than any other genetic variant or mutation. In Myc-335 null mice, Myc transcripts were expressed in the intestinal crypts in a pattern similar to that in wild-type mice but at modestly reduced levels. The mutant mice displayed no overt phenotype but were markedly resistant to intestinal tumorigenesis induced by the APCmin mutation. These results establish that a cancer-associated SNP identified in human genome-wide association studies has a functional effect in vivo. Exon-array analysis of mouse colon tissues from Myc-335 null and wild-type mouse (both mice are male and from the same litter). Related ChIP-seq data available in Short Read Archive, Accession ERP001919

2012-11-02 | E-GEOD-41219 | biostudies-arrayexpress

Mus musculus

Project description:Cardiac samples from OTT1 null/null and OTT1 null/wt embryonic mice

| PRJNA112799 | ENA

Transcription factor EBF1 non-cell autonomously regulates cardiac growth and differentiation

Project description:Reciprocal interactions between non-myocytes and cardiomyocytes are implicated in the control of cardiac growth and differentiation. Here, we report the identification of early B-cell factor 1 (Ebf1) as a transcription factor highly enriched in non-myocytes that potently regulates heart development. Postnatal Ebf1 deficient hearts are characterized by marked myocardial hypercellularity and reduced cardiomyocyte size, as well as ventricular conduction system hypoplasia and conduction system disease. Growth abnormalities in Ebf1 knockout hearts are observed as early as embryonic day 13.5, with dysregulated cell cycling, myocardial hyperplasia, and immature trabecular morphology. Transcriptional profiling of Ebf1-deficient non-myocytes isolated from embryonic hearts demonstrates dysregulation of Polycomb repressive complex 2 (PRC2) targets, while ATAC-Seq reveals differences in chromatin accessibility near many of these same genes. Gene set enrichment analysis of differentially expressed genes in cardiomyocytes isolated from E13.5 hearts of wildtype and Ebf1 deficientmice reveals significant enrichment of MYC targets, and consistent with this finding, we observe increased abundance of MYC in mutant hearts. Mechanistically, we show that EBF1-deficient non-myocytes, but not wildtype non-myocytes, are sufficient to induce excessive accumulation of nuclear-localized MYC protein in co-cultured wildtype cardiomyocytes. Finally, we demonstrate that BMP signaling induces Ebf1 expression in embryonic heart cultures and controls a gene program enriched in EBF1 targets. Taken together, these results reveal a novel non-cell autonomous pathway controlling cardiac growth and development.

2023-10-12 | GSE243167 | GEO

Analysis of myosin light chain migration pattern in 2D gels of human left ventricular proteins

Project description:The myosin light chain protein family consists of two classes, the regulatory myosin light chains (RLC) and the essential myosin light chains (ELC). Functionally, the MLC proteins are directly involved in sarcomeric activity and force transmission contributing to cardiac contractility. Besides regulating contractility by protein-protein interactions alone, MLCs modulate force transmission through posttranslational phosphorylation. The MLC phosphorylation status in human cardiac disease is under investigation. In contrast to RLC, the phosphorylation pattern of ELC in human heart disease is not well understood. Here, 2-dimensional (2D) gel electrophoresis followed by ELC specific immunoblot (IB) was performed to detect the ELC phosphorylation pattern of human left ventricular tissue. Cardiac proteins were separated by isoelectric point (pI) and molecular weight (MW) (vELC: MW 21,932 kDa, pI 5.03; vRLC: MW 19 kDa, pI 4.89). Next, we performed mass-spectrometry analysis after cutting the spot-regions in question from silver-stained 2D gels of proteins from the human tissue. The aim was 1) to validate the detection of the MLC migration pattern seen in 2D IB by mass spectrometry, 2) to distinguish between atrial and ventricular MLC isoforms as these two forms might converge on 2D gel (vELC: MW 21.932 kDa, pI 5.03; aELC: 21.550 kDa, pI 4.98) and 3) to detect phosphorylated amio acid residues of ELC and RLC in human ventricular tissue.

2022-07-24 | PXD033908 | Pride

DNMT3B7 disrupts embryonic development and accelerates lymphomagenesis

Project description:Cancer cells have an altered distribution of DNA methylation and express aberrant DNA methyltransferase 3B transcripts, which encode truncated proteins. To test if a truncated DNMT3B isoform disrupts DNA methylation in vivo, we constructed transgenic mice expressing DNMT3B7, a common truncated DNMT3B isoform in cancer cells. DNMT3B7 transgenic mice exhibit altered embryonic development, including lymphopenia, craniofacial abnormalities, and cardiac defects, similar to Dnmt3b-deficient animals, but rarely develop cancer. However, DNMT3B7 expression increases the frequency of mediastinal lymphomas in Eμ−myc animals. Eμ-myc/DNMT3B7 lymphomas have more chromosomal rearrangements, increased global methylation levels, and more locus-specific perturbations in DNA methylation patterns compared to Eμ-myc lymphomas. Our results demonstrate that a truncated DNMT3B protein can alter tumorigenesis, suggesting a similar role in human tumors. Direct comparison of DNA methylation in lymphoma samples from Eu-Myc vs Eu-Myc/Dnmt3b7 mice.

2010-07-30 | E-GEOD-21273 | biostudies-arrayexpress

Single cell transcriptomics reveal an essential role for Hippo signaling in cell state transitions during cardiac fibroblast development

Project description:We use single cell RNA-sequencing (Drop-seq) to profile cardiac cells (excluded atria) from control (Wt1 CreERT2/+; Rosa26mTmG/+) and epicardial-deficient Lats1/2 kinase embryonic hearts (Wt1 CreERT2/+; Lats1/2 F/F; Rosa26mTmG/+) at E13.5 and E14.5. Each experimental group includes cells sampled from four embryonic hearts.

2018-04-23 | GSE100861 | GEO

Whole transcriptome RNAseq analysis of germ cells in Inhba and Inha fetal testis

Project description:We performed bulk RNA-Seq on male fetal germ cells isolated from E13.5 and E15.5 testes from activin A-deficient mice (Inhba KO), and from E13.5 testes from mice with greater activin A bioactivity (Inha KO). The aim of this expereiment was to determine how chronic altered activin A bioactivity altered the germline transcriptome.

2022-05-26 | GSE201520 | GEO

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