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RNA-sequencing of differentiated mouse skeletal muscle cells following the depletion of EYA3

ABSTRACT: RNA-sequencing of differentiated mouse skeletal muscle cells following the depletion of EYA3

PROVIDER: PRJNA875428 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21377335_1.fastq.gz	Fastqsanger.gz
	SRR21377335_2.fastq.gz	Fastqsanger.gz
	SRR21377336_1.fastq.gz	Fastqsanger.gz
	SRR21377336_2.fastq.gz	Fastqsanger.gz
	SRR21377337_1.fastq.gz	Fastqsanger.gz

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RNA-sequencing of differentiated mouse skeletal muscle cells following the depletion of EYA3

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Project description:NAD is a ubiquitous electron carrier essential for energy metabolism and the post-translational modification of numerous regulatory proteins. Perturbation of NAD metabolism is considered detrimental to health, with NAD depletion commonly thought to promote aging. However, to what extent normal NAD concentration can be decreased without deleterious repercussions is unclear. Here, we describe a mouse model where NAMPT-mediated NAD+ biosynthesis is disrupted in adult skeletal muscle. The resulting 85% decrease in muscle NAD+ abundance did not cause tissue degeneration or dysfunction, as reflected in its unchanged morphology, contractility, and exercise tolerance. The lack of defects was corroborated by intact mitochondrial respiratory capacity and unaffected muscle transcriptomic and proteomic profiles. Furthermore, lifelong NAD depletion did not accelerate muscle aging or impair whole-body metabolism. Collectively, these findings demonstrate that NAD depletion does not drive the age-related decline in skeletal muscle function.

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Project description:NAD is a ubiquitous electron carrier essential for energy metabolism and the post translational modification of numerous regulatory proteins. Perturbation of NAD metabolism is considered detrimental to health, with NAD depletion commonly thought to promote aging. However, the extent to which cellular NAD concentration can be decreased without deleterious repercussions is unclear. We generated a mouse model where nicotinamide phosphoribosyltransferase (NAMPT)-mediated NAD+ biosynthesis is disrupted in adult skeletal muscle. The resulting 85% decrease in muscle NAD+ abundance was associated with preserved tissue integrity and functionality, as demonstrated by its unchanged morphology, contractility, and exercise tolerance. This lack of defects was corroborated by intact mitochondrial respiratory capacity and unaffected muscle transcriptomic and proteomic profiles. Furthermore, lifelong NAD depletion did not accelerate muscle aging or impair whole-body metabolism. Collectively, these findings indicate that NAD depletion does not contribute to age related declines in skeletal muscle function.

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Changes in skeletal muscle gene expression following castration

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NAD Depletion in Skeletal Muscle does not Compromise Muscle Function or Accelerate Aging

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