Muscle regeneration controlled by a designated DNA dioxygenase (Methylation-Seq)
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA666125 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12728605_1.fastq.gz | Fastqsanger.gz | |||
| SRR12728605_2.fastq.gz | Fastqsanger.gz | |||
| SRR12728606_1.fastq.gz | Fastqsanger.gz | |||
| SRR12728606_2.fastq.gz | Fastqsanger.gz |
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Project description:Muscle regeneration controlled by a designated DNA dioxygenase
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Project description:Muscle regeneration controlled by a designated DNA dioxygenase (RNA-Seq)
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Project description:Muscle regeneration controlled by a designated DNA dioxygenase (ATAC-Seq)
| PRJNA666126 | ENA
Project description:DNA methylation plays critical roles in regulating muscle cell fate determination and myogenesis. Tet dioxygenases are responsible for active DNA demethylation. The functions of Tet proteins in muscle regeneration have not been well characterized. Here we find that Tet2 is required for complete regeneration after muscle injury. Loss of Tet2 in myoblasts leads to reduced fusion index and thinner myofibers. Tet2 activates transcription of key differentiation modulator Myogenin (MyoG) further promoting myoblast differentiation and fusion. Re-expressing of MyoG in Tet2 KO myoblasts rescues the differentiation and fusion defects. Further mechanistic analysis reveals that Tet2 facilitates the recruitment of H3K4me1 and H3K27ac, increases the chromatin accessibility, and MyoD binding on MyoG enhancer. These functions are specifically executed by Tet2, but not Tet1 and Tet3. We identified the Tet2 specific function during myogenesis and shed new lights on DNA methylation and pioneer transcription factor transcription activation.
2021-06-01 | GSE158647 | GEO
Project description:DNA methylation plays critical roles in regulating muscle cell fate determination and myogenesis. Tet dioxygenases are responsible for active DNA demethylation. The functions of Tet proteins in muscle regeneration have not been well characterized. Here we find that Tet2 is required for complete regeneration after muscle injury. Loss of Tet2 in myoblasts leads to reduced fusion index and thinner myofibers. Tet2 activates transcription of key differentiation modulator Myogenin (MyoG) further promoting myoblast differentiation and fusion. Re-expressing of MyoG in Tet2 KO myoblasts rescues the differentiation and fusion defects. Further mechanistic analysis reveals that Tet2 facilitates the recruitment of H3K4me1 and H3K27ac, increases the chromatin accessibility, and MyoD binding on MyoG enhancer. These functions are specifically executed by Tet2, but not Tet1 and Tet3. We identified the Tet2 specific function during myogenesis and shed new lights on DNA methylation and pioneer transcription factor transcription activation.
2021-06-01 | GSE158646 | GEO
Project description:DNA methylation plays critical roles in regulating muscle cell fate determination and myogenesis. Tet dioxygenases are responsible for active DNA demethylation. The functions of Tet proteins in muscle regeneration have not been well characterized. Here we find that Tet2 is required for complete regeneration after muscle injury. Loss of Tet2 in myoblasts leads to reduced fusion index and thinner myofibers. Tet2 activates transcription of key differentiation modulator Myogenin (MyoG) further promoting myoblast differentiation and fusion. Re-expressing of MyoG in Tet2 KO myoblasts rescues the differentiation and fusion defects. Further mechanistic analysis reveals that Tet2 facilitates the recruitment of H3K4me1 and H3K27ac, increases the chromatin accessibility, and MyoD binding on MyoG enhancer. These functions are specifically executed by Tet2, but not Tet1 and Tet3. We identified the Tet2 specific function during myogenesis and shed new lights on DNA methylation and pioneer transcription factor transcription activation.
2021-06-01 | GSE158648 | GEO
Project description:Tet dioxygenases are responsible for the active DNA demethylation. The functions of Tet proteins in muscle regeneration have not been well characterized. Here we find that Tet2, but not Tet1 and Tet3, is specifically required for muscle regeneration in vivo. Loss of Tet2 leads to severe muscle regeneration defects. Further analysis indicates that Tet2 regulates myoblast differentiation and fusion. Tet2 activates transcription of the key differentiation modulator Myogenin (MyoG) by actively demethylating its enhancer region. Re-expressing of MyoG in Tet2 KO myoblasts rescues the differentiation and fusion defects. Further mechanistic analysis reveals that Tet2 enhances MyoD binding by demethylating the flanking CpG sites of E boxes to facilitate the recruitment of active histone modifications and increase chromatin accessibility and activate its transcription. These findings shed new lights on DNA methylation and pioneer transcription factor activity regulation.
| S-EPMC8149877 | biostudies-literature
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-06-01 | GSE158649 | GEO
Project description:MicroRNAs (miRNAs) are important in the regulation of many biological processes including muscle development. However, little is known regarding miRNA regulation of muscle regeneration. In mature murine tibialis anterior muscle following injury, 298 miRNAs were significantly changed during the time course of muscle regeneration including 86 that were altered greater than 10-fold as compared to uninjured muscle. Temporal miRNA expression patterns were identified and included inflammation-related miRNAs (miR-223 and -147) that increased immediately after injury; this pattern contrasted to that of mature muscle-specific miRNAs (miR-1, -133a and -499) that were abruptly decreased following injury and then up-regulated in later regenerative events. Another cluster of miRNAs were transiently increased in the early days of muscle regeneration. This included miR-351, a miRNA that was also transiently expressed during myogenic progenitor cell (MPC) differentiation in vitro. Based on computational predictions, further studies demonstrated that E2f3 was a target of miR-351 in myoblasts. Moreover, knockdown of miR-351 expression inhibited MPC proliferation and promoted apoptosis during MPC differentiation, whereas miR-351 overexpression protected MPC from apoptosis during differentiation. Collectively, these observations suggest that miR-351 is involved in both the maintenance of MPC proliferation and the transition of MPC into differentiated myotubes. Thus, a novel, time-dependent sequence of molecular events during skeletal muscle regeneration has been identified, i.e., miR-351 inhibits E2f3 expression, a key regulator of cell cycle progression and proliferation, and promotes MPC proliferation and protects early differentiating MPC from apoptosis, important events in the hostile tissue environment after acute muscle injury. Skeletal muscles are damaged and repaired repeatedly throughout life. Muscle regeneration maintains locomotor function during aging and delays the appearance of clinical symptoms in neuromuscular diseases, such as Duchenne muscular dystrophy. The capacity for skeletal muscle growth and regeneration is conferred by satellite cells located between the basal lamina and the sarcolemma of mature myofibers. Upon injury, satellite cells reenter the cell cycle, proliferate, and then exit the cell cycle either to renew the quiescent satellite cell pool or to differentiate into mature myofibers. Despite recent advances, genes involved in these processes are still largely unknown. Understanding the molecular mechanisms that regulate satellite cell activities could promote development of novel countermeasures to enhance muscle regeneration that is compromised by diseases or aging. Using a muscle injury mouse model, we profiled miRNA expression during muscle regeneration.
2012-04-24 | E-GEOD-37479 | biostudies-arrayexpress
Project description:Temporal expression profiling was utilized to define transcriptional regulatory pathways in vivo in a mouse muscle regeneration model. Potential downstream targets of MyoD were identified by temporal expression, promoter data base mining, and gel shift assays; Slug and calpain 6 were identified as novel MyoD targets. Slug, a member of the snail/slug family of zinc finger transcriptional repressors critical for mesoderm/ectoderm development, was further shown to be a downstream target by using promoter/reporter constructs and demonstration of defective muscle regeneration in Slug null mice.
2007-11-06 | E-GEOD-469 | biostudies-arrayexpress