EconPapers    
Economics at your fingertips  
 

Lsd1 regulates skeletal muscle regeneration and directs the fate of satellite cells

Milica Tosic, Anita Allen, Dominica Willmann, Christoph Lepper, Johnny Kim, Delphine Duteil and Roland Schüle ()
Additional contact information
Milica Tosic: Albert-Ludwigs-University Freiburg
Anita Allen: Albert-Ludwigs-University Freiburg
Dominica Willmann: Albert-Ludwigs-University Freiburg
Christoph Lepper: Carnegie Institution
Johnny Kim: Max Planck Institute for Heart and Lung Research
Delphine Duteil: Albert-Ludwigs-University Freiburg
Roland Schüle: Albert-Ludwigs-University Freiburg

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Satellite cells are muscle stem cells required for muscle regeneration upon damage. Of note, satellite cells are bipotent and have the capacity to differentiate not only into skeletal myocytes, but also into brown adipocytes. Epigenetic mechanisms regulating fate decision and differentiation of satellite cells during muscle regeneration are not yet fully understood. Here, we show that elevated levels of lysine-specific demethylase 1 (Kdm1a, also known as Lsd1) have a beneficial effect on muscle regeneration and recovery after injury, since Lsd1 directly regulates key myogenic transcription factor genes. Importantly, selective Lsd1 ablation or inhibition in Pax7-positive satellite cells, not only delays muscle regeneration, but changes cell fate towards brown adipocytes. Lsd1 prevents brown adipocyte differentiation of satellite cells by repressing expression of the novel pro-adipogenic transcription factor Glis1. Together, downregulation of Glis1 and upregulation of the muscle-specific transcription program ensure physiological muscle regeneration.

Date: 2018
References: Add references at CitEc
Citations: View citations in EconPapers (2)

Downloads: (external link)
https://www.nature.com/articles/s41467-017-02740-5 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02740-5

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/s41467-017-02740-5

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().

 
Page updated 2025-03-19
Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-017-02740-5