BMB Rep. 2016; 49(6): 303-304  
Novel function of stabilin-2 in myoblast fusion: the recognition of extracellular phosphatidylserine as a “fuse-me” signal
Go-Woon Kim1, Seung-Yoon Park1,2 & In-San Kim1,3,*
1Center for Theragnosis, Biomedical Research Institute, Korea Institute of Science and Technology (KIST), Seoul 02792, 2Department of Biochemistry, School of Medicine, Dongguk University, Gyeongju 38066, 3KU-KIST School, Korea University, Seoul 02841, Korea
Correspondence to: E-mail: iskim14@kist.re.kr
Received: May 7, 2016; Published online: June 30, 2016.
© Korean Society for Biochemistry and Molecular Biology. All rights reserved.

Abstract
Myoblast fusion is important for skeletal muscle formation. Even though the knowledge of myoblast fusion mechanism has accumulated over the years, the initial signal of fusion is yet to be elucidated. Our study reveals the novel function of a phosphatidylserine (PS) receptor, stabilin-2 (Stab2), in the modulation of myoblast fusion, through the recognition of PS exposed on myoblasts. During differentiation of myoblasts, Stab2 expression is higher than other PS receptors and is controlled by calcineurin/NFAT signaling on myoblasts. The forced expression of Stab2 results in an increase in myoblast fusion; genetic ablation of Stab2 in mice causes a reduction in muscle size, as a result of impaired myoblast fusion. After muscle injury, muscle regeneration is impaired in Stab2- deficient mice, resulting in small myofibers with fewer nuclei, which is due to reduction of fusion rather than defection of myoblast differentiation. The fusion-promoting role of Stab2 is dependent on its PS-binding motif, and the blocking of PS-Stab2 binding impairs cell-cell fusion on myoblasts. Given our previous finding that Stab2 recognizes PS exposed on apoptotic cells for sensing as an “eat-me” signal, we propose that PS-Stab2 binding is required for sensing of a “fuse-me” signal as the initial signal of myoblast fusion.
Keywords: Muscle regeneration, Myoblast fusion, Phosphatidylserine, Stabilin-2


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