Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA356295 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:We performed gene expression profiling by microarray using RNA extracted from the tibialis anterior of control and Hira myofiber-specific conditional knockout mice at 6 months of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed loci. Conditional knockout of Hira in myofibers improved strength and endurance, caused hypertrophy and regeneration, and increased the percentage of type I fibers. These results illustrate the physiological consequences of disrupting Hira-mediated chromatin assembly in myofibers.
2017-06-26 | GSE90900 | GEO
Project description:We performed gene expression profiling by microarray using RNA extracted from the tibialis anterior of control and Hira myofiber-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed loci. Conditional knockout of Hira in myofibers caused hypertrophy, degeneration, and increased the percentage of type I fibers. These results illustrate the physiological consequences of disrupting Hira-mediated chromatin assembly in myofibers.
2017-06-26 | GSE97359 | GEO
Project description:We performed gene expression profiling by microarray using RNA extracted from healthy free wall left ventricle tissues from control and Hira cardiomyocyte-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed regions. Conditional knockout of Hira in cardiomyocytes resulted in impaired cardiac function, cardiomyocyte degeneration and focal replacement fibrosis. These results illustrate the role of Hira in controlling the cardiac gene program. 4 animals per group (control and Hira conditional knockout) hybridized in triplicate. RNA was extracted from healthy free wall left ventricle.
2016-04-06 | E-GEOD-71833 | biostudies-arrayexpress
Project description:DNA methylation occurs as 5-methylcytosines mainly at cytosine-guanine dinucleotides, so-called CpG sites, and such methylation is a well-studied epigenetic mechanism for transcriptional regulation. Genomic DNA methylation patterns are established by the actions of the de novo methyltransferases Dnmt3a and Dnmt3b, and are maintained by the methyltransferase Dnmt1. Expression of Dnmt3a mRNA is relatively high in skeletal muscle, suggesting a major role in transcriptional regulation. Thus, we created transgenic mice specifically overexpressing Dnmt3a in skeletal muscle (Dnmt3a Tg mice). In this study, we performed a microarray analysis of skeletal muscle in wild-type control and Dnmt3a Tg mice (young: 3 months of age, female, and old: 26 months of age, female). The microarray data shows upregulation of a set of slow-twitch myofiber-specific genes and downregulation of fast-twitch myofiber-specific genes in Dnmt3a-Tg muscle compared with WT muscle.
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Project description:We performed gene expression profiling by microarray using RNA extracted from healthy free wall left ventricle tissues from control and Hira cardiomyocyte-specific conditional knockout mice at 6 weeks of age. Hira is a histone chaperone responsible for replication-independent incorporation of histone variant H3.3 at actively transcribed regions. Conditional knockout of Hira in cardiomyocytes resulted in impaired cardiac function, cardiomyocyte degeneration and focal replacement fibrosis. These results illustrate the role of Hira in controlling the cardiac gene program.
2016-04-06 | GSE71833 | GEO
Project description:To investigate the roles of ATF4 in skeletal muscle aging we generated muscle-specific ATF4 knockout (ATF4 mKO) mice. We then performed gene expression profiling analysis using data obtained from RNA-seq of tibialis anterior muscles at 6-months and 22-months of age.
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Project description:This study aims to characterize the diversity of cell types in human skeletal muscle across age using two complementary technologies: single-cell and single-nucleus sequencing, which provide a comprehensive coverage of cell types in the muscle. We leveraged the aforementioned datasets to study change in cell type composition and gene expression between young (n= 8, approx. 20-40 yrs) and old (n = 9, approx. 60-80 yrs) adults, highlighting changes in the major skeletal muscle compartments, muscle satellite cells, myofiber and muscle microenvironment including stromal, immune and vascular cell types. Additionally, we generated a complementary mouse muscle aging dataset by profiling hindlimb muscles from young (n = 5, 3 months) versus old mice (n = 3, 19 months), using single-cell and single-nucleus sequencing for comparison.
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Project description:Sarcopenia is a degenerative condition that consists in the age-induced atrophy and functional decline of skeletal muscle cells (myofibers). A common hypothesis is that inducing myofiber hypertrophy should also reinstate myofiber contractile function but such model has not been extensively tested. Here, we find that the levels of the ubiquitin ligase UBR4 increase in skeletal muscle with aging, and that muscle-specific UBR4 loss rescues age-associated myofiber atrophy in mice. However, UBR4 promotes proteolysis by the proteasome and consequently UBR4 loss reduces the muscle specific force and accelerates the decline in muscle protein quality that occurs with aging in mice. Similarly, hypertrophic signaling induced via muscle-specific loss of UBR4 and of several other ubiquitin ligases consistently compromises muscle function and shortens lifespan in Drosophila by reducing protein quality control. Altogether, these findings indicate that ubiquitin ligases regulate in opposite fashion myofiber size and muscle protein quality control during aging.
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Project description:Sarcopenia, characterized by the loss of muscle mass, strength, and function, predisposes adverse outcomes and its mechanism is waiting to reveal. Here, we report decrease of PRR14, a nuclear protein, in skeletal muscle results in sarcopenia. Genetically, genome-wide association studies (GWAS) identified multiple single nucleotide polymorphisms (SNPs) in PRR14 locus associated with body mass index (BMI) and total body lean mass, which indicated its association with sarcopenia; Specific knockout of skeletal muscle Prr14 in mice confirmed the causal effect; Biochemical analysis and high-throughput sequencing, including both transcriptome and approaches for the study of the epigenome (CUT&Tag sequencing and ATAC sequencing), revealed that Prr14 was required for myofiber homeostasis in skeletal muscle: Prr14 loss altered chromatin structure and reduced Mef2c activity, which in combination resulted in failure of maintaining myofiber identity and therefore sarcopenia. Our findings demonstrate that PRR14 orchestrates critical epigenetic changes and transcription factor activity to maintain myofiber identity, thereby providing novel therapeutic avenues for skeletal muscle pathologies associated with dysregulation of these mechanisms.
2024-12-23 | GSE243332 | GEO
Project description:Sarcopenia, characterized by the loss of muscle mass, strength, and function, predisposes adverse outcomes and its mechanism is waiting to reveal. Here, we report decrease of PRR14, a nuclear protein, in skeletal muscle results in sarcopenia. Genetically, genome-wide association studies (GWAS) identified multiple single nucleotide polymorphisms (SNPs) in PRR14 locus associated with body mass index (BMI) and total body lean mass, which indicated its association with sarcopenia; Specific knockout of skeletal muscle Prr14 in mice confirmed the causal effect; Biochemical analysis and high-throughput sequencing, including both transcriptome and approaches for the study of the epigenome (CUT&Tag sequencing and ATAC sequencing), revealed that Prr14 was required for myofiber homeostasis in skeletal muscle: Prr14 loss altered chromatin structure and reduced Mef2c activity, which in combination resulted in failure of maintaining myofiber identity and therefore sarcopenia. Our findings demonstrate that PRR14 orchestrates critical epigenetic changes and transcription factor activity to maintain myofiber identity, thereby providing novel therapeutic avenues for skeletal muscle pathologies associated with dysregulation of these mechanisms.
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