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Mus musculus

ABSTRACT: Project title: Gene expression data from Control and Setd7 KO cultured skeletal muscle stem cells

PROVIDER: PRJNA407978 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6079340_1.fastq.gz	Fastqsanger.gz
	SRR6079340_2.fastq.gz	Fastqsanger.gz
	SRR6117037_1.fastq.gz	Fastqsanger.gz
	SRR6117037_2.fastq.gz	Fastqsanger.gz
	SRR6117018_1.fastq.gz	Fastqsanger.gz

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Project description:H3K4me1 ChIPSeq data from cultured skeletal muscle stem cells treated with/without Setd7 inhibitor (R)-PFI-2.

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Project description:Following skeletal muscle injury, muscle stem cells (satellite cells) are activated, proliferate, and differentiate to form myofibers. We show that mRNA decay protein AUF1 regulates satellite cell function through targeted degradation of specific mRNAs. AUF1 targets certain mRNAs containing 3 AU-rich elements (AREs) for rapid decay. Auf1-/- (KO) mice undergo accelerated skeletal muscle wasting with age and impaired muscle repair following injury. Satellite cell mRNA analysis and regeneration studies demonstrate that auf1-/- satellite cell self-renewal is impaired due to increased stability and overexpression of ARE-mRNAs. Control of ARE-mRNA decay by AUF1 and potentially other ARE-binding proteins represents a mechanism for adult stem cell regulation and is implicated in human muscle wasting diseases. We report the RNA transcript expression profiles from sorted satellite cells isolated from wild type (WT) and AUF1-null (KO) mice hindlimb muscles Examination of RNA transcript expression from satellite cells of two genotypes Please note that mice are bred through a C57BL/6 strain of 129 background.

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WT and AUF1 KO satellite cell RNA-sequencing

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Project description:MicroRNA-1 (miR-1) is the most abundant miRNA in adult skeletal muscle. To determine the function of miR-1 in adult skeletal muscle, we generated an inducible, skeletal muscle-specific miR-1 knockout (KO) mouse. Integration of RNA-sequencing (RNA-seq) data from miR-1 KO muscle with Argonaute 2 enhanced crosslinking and immunoprecipitation sequencing (AGO2 eCLIP-seq) from human skeletal muscle identified miR-1 target genes involved with glycolysis and pyruvate metabolism. The loss of miR-1 in skeletal muscle induced cancer-like metabolic reprogramming, as shown by higher pyruvate kinase muscle isozyme M2 (PKM2) protein levels, which promoted glycolysis. Comprehensive bioenergetic and metabolic phenotyping combined with skeletal muscle proteomics and metabolomics further demonstrated that miR-1 KO induced metabolic inflexibility as a result of pyruvate oxidation resistance. While the genetic loss of miR-1 reduced endurance exercise performance in mice and in C. elegans, the physiological down-regulation of miR-1 expression in response to a hypertrophic stimulus in both humans and mice may cause a similar metabolic reprogramming that supports muscle cell growth. Taken together, these data identify a novel post-translational mechanism of adult skeletal muscle metabolism regulation mediated by miR-1.

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Project description:To investigate the role of the circadian clock gene Bmal1 in skeletal muscle, we compared the circadian transcriptomes of fast tibialis anterior (TA) and slow soleus (SOL) skeletal muscles from muscle-specific Bmal1 KO (mKO) and their control Cre- littermates (Ctrl). Keyword: Circadian Transcriptome, time course

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Transcription profiling of p68/72 deficient C2C12 cells cultured in either growth medium or differentiation medium to investigate the function of p68/p72 in muscle gene expression and skeletal C2C12 cell differentiation.

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