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Enhancer Profiling Reveals Regulators of Skeletal Muscle Identity and Reprogramming [ATAC-seq]

ABSTRACT: Chromatin immunoprecipitation sequencing of H3K4me2, H3K27ac as well as, ATACseq and RNA-seq reveals regulatory landscapes across different muscle groups, as well as in response to chronic exercise or muscle PGC1a overexpression. This work defines the unique enhancer repetoire of skeletal muscle in vivo and reveals that highly divergent exercise-induced or PGC1a-driven epigenomic programs direct partially convergent transcriptional networks.

ORGANISM(S): Mus musculus

PROVIDER: GSE134962 | GEO | 2019/09/10

REPOSITORIES: GEO

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Enhancer Profiling Reveals Regulators of Skeletal Muscle Identity and Reprogramming [ChIP-Seq]

Project description:Chromatin immunoprecipitation sequencing of H3K4me2, H3K27ac as well as, ATACseq and RNA-seq reveals regulatory landscapes across different muscle groups, as well as in response to chronic exercise or muscle PGC1a overexpression. This work defines the unique enhancer repetoire of skeletal muscle in vivo and reveals that highly divergent exercise-induced or PGC1a-driven epigenomic programs direct partially convergent transcriptional networks.

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Enhancer Profiling Reveals Regulators of Skeletal Muscle Identity and Reprogramming [RNA-seq]

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Enhancer Profiling Reveals Regulators of Skeletal Muscle Identity and Reprogramming [ChIP-seq, ATAC-seq]

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Impact of short and long-term electrically induced muscle exercise on gene signaling pathways, gene expression, and PGC1a methylation in men with spinal cord injury

Project description:Exercise attenuates the development of chronic non-communicable diseases (NCDs). Gene signaling pathway analysis offers an opportunity to discover if electrically induced muscle exercise regulates key pathways among people living with spinal cord injury (SCI). We examined short-term and long-term durations of electrically induced skeletal muscle exercise on complex gene signaling pathways, specific gene regulation, and epigenetic tagging of PGC1a, a major transcription factor in skeletal muscle of men with SCI. After short or long-term electrically induced exercise training, participants underwent biopsies of the trained and untrained muscles. RNA was hybridized to an exon microarray and analyzed using a gene set enrichment analysis. We discovered that long-term exercise training regulated the Reactome gene sets for Metabolism (38 gene sets), Cell Cycle (36 gene sets), Disease (27 gene sets), Gene Expression and Transcription (22 gene sets), Organelle Biogenesis (4 gene sets), Cellular Response to Stimuli (8 gene sets), Immune System (8 gene sets), Vesicle Mediated Transport (4 gene sets), and Transport of Small Molecules (3 gene sets). Specific gene expression included: Oxidative catabolism of glucose including PDHB (p<0.001), PDHX (p<0.001), MPC1 (p<0.009), and MPC2 (p<0.007); Oxidative phosphorylation genes including SDHA (p<0.006), SDHB (p<0.001), NDUFB1 (p<0.002), NDUFA2 (p<0.001); Transcription Genes including PGC1α (p<0.030) and PRKAB2 (p<0.011); Hypertrophy gene MSTN (p<0.001); and the Myokine generating FNDC5 gene (p<0.008). Long-term electrically induced exercise de-methylated the major transcription factor, PGC1a. Taken together, these findings support that long term electrically induced muscle activity regulates key pathways associated with muscle health and systemic metabolism.

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Expression data from quadriceps muscle of WT and ERRgamma transgenic mice

Project description:We show that the orphan nuclear receptor ERRg is expressed at high levels in type I muscle and when transgenically expressed in anaerobic type II muscles (ERRGO mice) or cultured cells, powerfully regulates VEGF expression, angiogenesis and vascular supply in absence of exercise. ERRGO mice show increased expression of genes promoting fat metabolism, mitochondrial respiration and type I fiber specification. In parallel, the type II muscle in ERRGO mice display an activated angiogenic program marked by myofibrillar induction and secretion of pro-angiogenic factors, frank neo-vascularization and a 100% increase in running endurance. Surprisingly, the induction of VEGF and type I muscle properties by ERRg does not involve the transcriptional co-activator PGC1a. Instead, ERRg genetically activates the energy sensor AMPK which is typically inactive in absence of exercise. Therefore, ERRg and AMPK, known regulators of mitochondrial function and metabolism, together control a novel angiogenic pathway that anatomically synchronizes vascular arborization to oxidative metabolism revealing an exercise-independent mechanism for matching supply and demand. Keywords: ERRgamma overexpression compared to wild-type Comparison of gene expression from quadriceps muscles isolated from wild type and alpha-skeletal actin-ERRgamma-transgenic mice.

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PGC1a and Exercise Adaptations in Zebrafish

Project description:PGC1a and Exercise Adaptations in Zebrafish

| PRJNA474826 | ENA

Expression data from quadriceps muscle of WT and ERRgamma transgenic mice

2011-09-19 | GSE22086 | GEO

Molecular control of endurance training adaptation in mouse skeletal muscle

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Satellite cell depletion results in a cryptic subpopulation of myonuclei in response to exercise

Project description:Skeletal muscle is composed of post-mitotic myofibers that form a syncytium containing hundreds of myonuclei. Using a progressive exercise training model in the mouse and single nucleus RNA-sequencing (snRNA-seq) for high resolution characterization of myonuclear transcription, we show myonuclear functional specialization in muscle from sedentary mice that is altered by 4 weeks of exercise training. Furthermore, in response to exercise, snRNA-seq reveals that resident muscle stem cells, satellite cells, were activated, but demonstrated limited lineage progression while contributing to muscle adaption. In the absence of satellite cells, trajectory analysis predicts the emergence of cryptic myonuclei that appear to lose their canonical identity. These data illustrate how myonuclear adaptation to exercise may be disrupted under conditions satellite cell compromise.

2021-07-17 | GSE162307 | GEO

Loss of ARNT Impair Adaptability of Muscular Exercise in Aged Mice

Project description:The adaptation of regimented exercise in skeletal muscle including muscular hypertrophy and enhanced strength decline significantly with aging. Transcriptome analysis following RNA sequencing reveals extensive activation of hypoxia-related genes in young exercised mice versus the sedentary, but absent in aged exercised mice. Particularly, less expression of aryl hydrocarbon receptor translocator (ARNT) was observed in response to exercise in aged mice. Young mice underwent skeletal muscle-specific knockout of ARNT (ARNT mKO) obtain deficient benefit from exercise resembling the aged mice. The deletion of ARNT associated with decreased expression of Notch1 intracellular domain(N1ICD) impair muscle hypertrophy and regeneration. Administration of ML228, a systematic agonist of ARNT, rescued skeletal muscle adaptabilities in old mice, which was suppressed by administrating N1ICD inhibitor(DAPT). These results suggest that the loss of skeletal muscle ARNT is partially responsible for diminished response to exercise in aging and activation of hypoxia signaling holds promise for rescuing the adaptability in aged muscle.

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