Somatic mutagenesis in satellite cells associates with human skeletal muscle aging

Nature Communications
Irene FrancoMaria Eriksson

Abstract

Human aging is associated with a decline in skeletal muscle (SkM) function and a reduction in the number and activity of satellite cells (SCs), the resident stem cells. To study the connection between SC aging and muscle impairment, we analyze the whole genome of single SC clones of the leg muscle vastus lateralis from healthy individuals of different ages (21-78 years). We find an accumulation rate of 13 somatic mutations per genome per year, consistent with proliferation of SCs in the healthy adult muscle. SkM-expressed genes are protected from mutations, but aging results in an increase in mutations in exons and promoters, targeting genes involved in SC activity and muscle function. In agreement with SC mutations affecting the whole tissue, we detect a missense mutation in a SC propagating to the muscle. Our results suggest somatic mutagenesis in SCs as a driving force in the age-related decline of SkM function.

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Methods Mentioned

BETA
biopsies
PCR
deamination
biopsy
RNA seq
fluorescence-activated cell sorting
genotyping
PCA

Software Mentioned

MATLAB
Fermikit
GATK RealignerTargetCreator
GATK HaplotypeCaller
package
FANTOM
Ensembl Effector Predictor
MuTect2 GATK
GraphPad Prism
Ensemble

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