Somatic mutagenesis in satellite cells associates with human skeletal muscle aging

Irene Franco (), Anna Johansson, Karl Olsson, Peter Vrtačnik, Pär Lundin, Hafdis T. Helgadottir, Malin Larsson, Gwladys Revêchon, Carla Bosia, Andrea Pagnani, Paolo Provero, Thomas Gustafsson, Helene Fischer and Maria Eriksson ()
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Irene Franco: Karolinska Institutet
Anna Johansson: Uppsala University
Karl Olsson: Karolinska Institutet
Peter Vrtačnik: Karolinska Institutet
Pär Lundin: Karolinska Institutet
Hafdis T. Helgadottir: Karolinska Institutet
Malin Larsson: Linköping University
Gwladys Revêchon: Karolinska Institutet
Carla Bosia: Italian Institute for Genomic Medicine (IIGM)
Andrea Pagnani: Italian Institute for Genomic Medicine (IIGM)
Paolo Provero: Molecular Biotechnology Center
Thomas Gustafsson: Karolinska Institutet
Helene Fischer: Karolinska Institutet
Maria Eriksson: Karolinska Institutet

Nature Communications, 2018, vol. 9, issue 1, 1-12

Abstract: 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.

Date: 2018
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DOI: 10.1038/s41467-018-03244-6

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