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Machado L, Relaix F. Heterochromatin compaction is regulated by Suv4-20h1 to maintains skeletal muscle stem cells quiescence. Stem Cell Investig. 2016;3:23doi: 10.21037/sci.2016.06.04.
Machado, L., & Relaix, F. (2016). Heterochromatin compaction is regulated by Suv4-20h1 to maintains skeletal muscle stem cells quiescence. Stem cell investigation, 323. https://doi.org/10.21037/sci.2016.06.04
Machado, Léo, and Relaix, Frédéric. "Heterochromatin compaction is regulated by Suv4-20h1 to maintains skeletal muscle stem cells quiescence." Stem cell investigation vol. 3 (2016): 23. doi: https://doi.org/10.21037/sci.2016.06.04
Machado L, Relaix F. Heterochromatin compaction is regulated by Suv4-20h1 to maintains skeletal muscle stem cells quiescence. Stem Cell Investig. 2016 Jun 20;3:23. doi: 10.21037/sci.2016.06.04. eCollection 2016. PMID: 27488816; PMCID: PMC4958057.
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Stem Cell Investig. 2016 Jun 20;3:23. doi: 10.21037/sci.2016.06.04. eCollection 2016.

Heterochromatin compaction is regulated by Suv4-20h1 to maintains skeletal muscle stem cells quiescence.

Stem cell investigation

Léo Machado, Frédéric Relaix

Affiliations

  1. 1 Inserm, IMRB U955-E10, 94000, Créteil, France ; 2 Faculté de Médecine, Université Paris Est Créteil, 94000, Créteil, France ; 3 Ecole Nationale Vétérinaire d'Alfort, 94700, Maisons-Alfort, France ; 4 Etablissement Francais du Sang, 94017, Créteil, France ; 5 APHP, Hopital Henri Mondor, DHU Pepsy & Centre de Référence des Maladies Neuromusculaires GNMH, 94000, Créteil, France.

PMID: 27488816 PMCID: PMC4958057 DOI: 10.21037/sci.2016.06.04

Abstract

In this report, Boonsanay and colleagues describe a novel mechanism of maintenance of skeletal muscle stem cells [also known as satellite cells (SCs)] quiescence via the di-methyltransferase Suv4-20h1, regulator of heterochromatin formation. Conditional ablation of Suv4-20h1 in SCs leads notably to the loss of the histone modification H4K20me2 on the distal regulatory element of Myod combined with a relocation of the Myod locus toward a central position in the nucleus. This switch in nuclear compartment is correlated with decreased facultative H3K27me3 associated heterochromatin, and an increase in spontaneously activated MYOD-expressing SCs in homeostatic muscles. Consequently, Suv4-20h1 knock-out SCs demonstrate compromised stem cell potential, as they fail to efficiently self-renew and replenish the SC pool upon muscle injury. Strikingly, restoring MYOD expression alone rescues the levels of facultative chromatin and reverses the loss-of-quiescence phenotype.

Keywords: H3K27me3; MYOD; Suv4-20h1; muscle regeneration; muscle stem cells; quiescence

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