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Myostatin promotes the terminal differentiation of embryonic muscle progenitors

¹ Developmental Biology Institute of Marseille Luminy (IBDML), CNRS UMR 6216, Université de la Méditerranée, Campus de Luminy, 13288 Marseille Cedex 09, France; ² Genetics of Development and Disease Branch, The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)/National Institutes of Health, Bethesda, Maryland 20892, USA; ³ Laboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA

Myostatin, a TGF-β family member, is an important regulator of adult muscle size. While extensively studied in vitro, the mechanisms by which this molecule mediates its effect in vivo are poorly understood. We addressed this question using chick and mouse embryos. We show that while myostatin overexpression in chick leads to an exhaustion of the muscle progenitor population that ultimately results in muscle hypotrophy, myostatin loss of function in chick and mouse provokes an expansion of this population. Our data demonstrate that myostatin acts in vivo to regulate the balance between proliferation and differentiation of embryonic muscle progenitors by promoting their terminal differentiation through the activation of p21 and MyoD. Previous studies have suggested that myostatin imposes quiescence on muscle progenitors. Our data suggest that myostatin’s effect on muscle progenitors is more complex than previously realized and is likely to be context-dependent. We propose a novel model for myostatin mode of action in vivo, in which myostatin affects the balance between proliferation and differentiation of embryonic muscle progenitors by enhancing their differentiation.

[Keywords: Myostatin; skeletal muscle; embryo; p21]]

Received August 28, 2007; revised version accepted December 19, 2007.

⁵ Corresponding author.

E-MAIL marcelle{at}ibdm.univ-mrs.fr; FAX 33-4-91-82-06-82.

Supplemental material is available at http://www.genesdev.org.

Article is online at http://www.genesdev.org/cgi/doi/10.1101/gad.454408.

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