RNA-Seq of juvenile and early adolescent muscle
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE121278 | GEO | 2018/10/16
REPOSITORIES: GEO
Similar Datasets
Project description:Purpose: During postnatal development the fetal skeletal muscle undergoes a rapid and dramatic transition to adult function through transcriptional and post-transcriptional mechanisms, including alternative splicing (AS) Methods:We performed RNA-seq for high-resolution analysis of transcriptome changes during postnatal mouse skeletal muscle development using RNA from gastrocnemius muscle from embryonic day 18.5, postnatal day 2 (PN2), PN14, PN28, adult (22 weeks). Results: We identified a novel role for AS in several cellular functions including calcium handling and membrane organization during postnatal skeletal muscle development. Furthermore, AS transitions within calcium handling genes are responsive to Celf1 and Mbnl1, RNA-binding proteins with developmentally regulated expression. Conclusions: We identified a novel role for AS in several functional categories during postnatal development including calcium handling, vesicular trafficking and cell junctions.
2017-12-22 | GSE108402 | GEO
Project description:Many genes responsive to C. citratus oil and citronellal were stress-related and they include genes associated with adrenergic signalling/calcium channels, cGMP-PKG signaling, apoptosis, focal adhesion, ECM-receptor interaction, ubiquitin mediated proteolysis, mTOR signalling pathway, and longevity regulating pathway.
2021-06-08 | GSE176275 | GEO
Project description:The Mediator complex regulates gene transcription by linking basal transcriptional machinery with DNA-bound transcription factors. The activity of the Mediator complex is mainly controlled by a kinase submodule that is comprised of four proteins, including MED12. Although ubiquitously expressed, Mediator subunits can differentially regulate gene expression in a tissue-specific manner. Here, we report that MED12 is required for normal cardiac function such that mice with conditional cardiac-specific deletion of MED12 display progressive dilated cardiomyopathy. Loss of MED12 perturbs expression of calcium handling genes in the heart, consequently altering calcium cycling in cardiomyocytes and disrupting cardiac electrical activity. We identified transcription factors that regulate expression of calcium-handling genes that are downregulated in the heart in the absence of MED12, and found that MED12 localizes to transcription factor consensus sequences within calcium handling genes. We showed that MED12 interacts with one such transcription factor, MEF2, in cardiomyocytes, and that MED12 and MEF2 co-occupy promoters of calcium handling genes. Furthermore, we demonstrated that MED12 enhances MEF2 transcriptional activity and overexpression of both increases expression of calcium handling genes in cardiomyocytes. Our data support a role for MED12 as a coordinator of transcription through MEF2 and other transcription factors. We conclude that MED12 is a regulator of a network of calcium handling genes, consequently “mediating” contractility in the mammalian heart.
2017-08-11 | GSE100088 | GEO
Project description:The Mediator complex regulates gene transcription by linking basal transcriptional machinery with DNA-bound transcription factors. The activity of the Mediator complex is mainly controlled by a kinase submodule that is comprised of four proteins, including MED12. Although ubiquitously expressed, Mediator subunits can differentially regulate gene expression in a tissue-specific manner. Here, we report that MED12 is required for normal cardiac function such that mice with conditional cardiac-specific deletion of MED12 display progressive dilated cardiomyopathy. Loss of MED12 perturbs expression of calcium handling genes in the heart, consequently altering calcium cycling in cardiomyocytes and disrupting cardiac electrical activity. We identified transcription factors that regulate expression of calcium-handling genes that are downregulated in the heart in the absence of MED12, and found that MED12 localizes to transcription factor consensus sequences within calcium handling genes. We showed that MED12 interacts with one such transcription factor, MEF2, in cardiomyocytes, and that MED12 and MEF2 co-occupy promoters of calcium handling genes. Furthermore, we demonstrated that MED12 enhances MEF2 transcriptional activity and overexpression of both increases expression of calcium handling genes in cardiomyocytes. Our data support a role for MED12 as a coordinator of transcription through MEF2 and other transcription factors. We conclude that MED12 is a regulator of a network of calcium handling genes, consequently “mediating” contractility in the mammalian heart.
2017-08-11 | GSE100087 | GEO
Project description:YAP transcriptional regulator controls cell mechanics by activating genes involved in cell-matrix interaction following extracellular matrix (ECM) remodelling and stiffening. YAP is needed for cardiogenesis in mouse but is repressed in adult cardiomyocytes. The protein is reactivated following ischemic insults, although the timing and mechanisms underlying YAP depletion during heart development and the reason for its reactivation are unclear. Here, we combine pluripotent stem cell (PSC) cardiac differentiation, mouse embryo development and human heart tissue analysis to demonstrate that the fine-tuning of cell mechanics, as controlled by YAP multiphasic activation through TEAD transcription, is crucial for mesoderm commitment and cardiac progenitor specification. Finally, by adopting induced PSC models of dilated cardiomyopathy, we prove that YAP-TEAD reactivation in diseased cardiomyocytes empowers calcium handling apparatus and increases cell contractility. Given YAP prompt activation following myocardial infarction, we unveil a novel role for mechanosensing in connecting ECM remodelling to cardiomyocyte function in pathological heart.
2020-10-30 | E-MTAB-7619 | biostudies-arrayexpress
Project description:YAP transcriptional regulator controls cell mechanics by activating genes involved in cell-matrix interaction following extracellular matrix (ECM) remodelling and stiffening. YAP is needed for cardiogenesis in mouse but is repressed in adult cardiomyocytes. The protein is reactivated following ischemic insults, although the timing and mechanisms underlying YAP depletion during heart development and the reason for its reactivation are unclear. Here, we combine pluripotent stem cell (PSC) cardiac differentiation, mouse embryo development and human heart tissue analysis to demonstrate that the fine-tuning of cell mechanics, as controlled by YAP multiphasic activation through TEAD transcription, is crucial for mesoderm commitment and cardiac progenitor specification. Finally, by adopting induced PSC models of dilated cardiomyopathy, we prove that YAP-TEAD reactivation in diseased cardiomyocytes empowers calcium handling apparatus and increases cell contractility. Given YAP prompt activation following myocardial infarction, we unveil a novel role for mechanosensing in connecting ECM remodelling to cardiomyocyte function in pathological heart.
2020-10-30 | E-MTAB-7620 | biostudies-arrayexpress
Project description:Postnatal handling in rodents leads to decreased anxiety-like behavior in adulthood. We used microarrays to look at gene expression differences in the CA1 region of the hippocampus in female mice subjected to postnatal handling compared to controls.
2008-10-08 | GSE11679 | GEO
Project description:Purpose: The aim of the study was to decipher the function of Creld1 in the myocardium during embryonic and postnatal heart development. Methods: We generated conditional knockout (KO) mice lacking Creld1 in cells expressing the Myosine Heavy Chain (MyHC, myocardial cells). Embryonic (E13.5, n=4) and postnatal (P3, n=3) hearts from both wild-type (WT) and KO mice were isolated and postnatal hearts were further split into atria and ventricles. Total RNA was extracted, mRNA purified, converted into cDNA and sequenced using a NextSeq500 system (Illumina).The reads passing default quality filters were aligned to the mouse genome (mm10). Results: More than 5.1 million aligned reads were retrieved in each sample.The expression profiles of the postnatal KO samples underline drastic anormalies in the hearts and commencing heart failure particularly in the atria. In embryonic KO hearts the transciption of Notch1 signalling components and consequently extracellular matrix (ECM) homeostasis was altered, whereas transcription in Nfatc1 and Vegf signalling pathways was unchanged. Conclusion: This study shows that myocardial Creld1 is a key morphogenic factor in the developing heart and as it regulates Notch1 signalling and, thereby, the ECM during cardiac wall development.
2023-05-30 | GSE159187 | GEO
Project description:Gene expression changes related to postnatal handling
| PRJNA106081 | ENA
Project description:We report that ablation of one SLN allele positively affects mouse mdx DMD heart failure model mice by several metrics including intracellular calcium handling.
2020-11-24 | GSE144596 | GEO