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Development. 2013 Sep;140(18):3743-53. doi: 10.1242/dev.095810. Epub 2013 Aug 14.

Dual role of delta-like 1 homolog (DLK1) in skeletal muscle development and adult muscle regeneration.

Author information

1
Laboratory of Molecular and Cellular Cardiology, Department of Clinical Biochemistry and Pharmacology, Odense University Hospital, Winsloewparken 21 3rd, 5000 Odense C, Denmark.

Abstract

Muscle development and regeneration is tightly orchestrated by a specific set of myogenic transcription factors. However, factors that regulate these essential myogenic inducers remain poorly described. Here, we show that delta-like 1 homolog (Dlk1), an imprinted gene best known for its ability to inhibit adipogenesis, is a crucial regulator of the myogenic program in skeletal muscle. Dlk1(-/-) mice were developmentally retarded in their muscle mass and function owing to inhibition of the myogenic program during embryogenesis. Surprisingly however, Dlk1 depletion improves in vitro and in vivo adult skeletal muscle regeneration by substantial enhancement of the myogenic program and muscle function, possibly by means of an increased number of available myogenic precursor cells. By contrast, Dlk1 fails to alter the adipogenic commitment of muscle-derived progenitors in vitro, as well as intramuscular fat deposition during in vivo regeneration. Collectively, our results suggest a novel and surprising dual biological function of DLK1 as an enhancer of muscle development, but as an inhibitor of adult muscle regeneration.

KEYWORDS:

Delta-like 1 homolog; Mouse; Muscle development; Muscle regeneration; Muscle stem cells

PMID:
23946446
DOI:
10.1242/dev.095810
[Indexed for MEDLINE]
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