miR-205 Regulates the Fusion of Porcine Myoblast by Targeting the Myomaker Gene

Author:

Ma Jideng1234,Zhu Yan4ORCID,Zhou Xiankun4,Zhang Jinwei123,Sun Jing123,Li Zhengjie4ORCID,Jin Long4ORCID,Long Keren4,Lu Lu4ORCID,Ge Liangpeng1235

Affiliation:

1. Chongqing Academy of Animal Sciences, Chongqing 402460, China

2. Key Laboratory of Pig Industry Sciences, Ministry of Agriculture, Chongqing 402460, China

3. Chongqing Key Laboratory of Pig Industry Sciences, Chongqing 402460, China

4. Farm Animal Genetic Resource Exploration and Innovation Key Laboratory of Sichuan Province, Sichuan Agricultural University, Chengdu 611130, China

5. Technical Engineering Center for the Development and Utilization of Medical Animal Resources, Chongqing 402460, China

Abstract

Skeletal muscle formation is an extremely important step in animal growth and development. Recent studies have found that TMEM8c (also known as Myomaker, MYMK), a muscle-specific transmembrane protein, can promote myoblast fusion and plays a key role in the normal development of skeletal muscle. However, the effect of Myomaker on porcine (Sus scrofa) myoblast fusion and the underlying regulatory mechanisms remain largely unknown. Therefore, in this study, we focused on the role and corresponding regulatory mechanism of the Myomaker gene during skeletal muscle development, cell differentiation, and muscle injury repair in pigs. We obtained the entire 3′ UTR sequence of porcine Myomaker using the 3′ RACE approach and found that miR-205 inhibited porcine myoblast fusion by targeting the 3′ UTR of Myomaker. In addition, based on a constructed porcine acute muscle injury model, we discovered that both the mRNA and protein expression of Myomaker were activated in the injured muscle, while miR-205 expression was significantly inhibited during skeletal muscle regeneration. The negative regulatory relationship between miR-205 and Myomaker was further confirmed in vivo. Taken together, the present study reveals that Myomaker plays a role during porcine myoblast fusion and skeletal muscle regeneration and demonstrates that miR-205 inhibits myoblast fusion through targeted regulation of the expression of Myomaker.

Funder

National Key R & D Program of China

National Natural Science Foundation of China

Major Science and Technology Projects of Tibet Autonomous Region

Sichuan Science and Technology Program

Special Support for Postdoctoral Research Projects of Chongqing

Municipal Financial Special Fund of Chongqing Academy of Animal Science

Performance Incentive Guidance for Scientific Research Institution of Chongqing

China Agriculture Research System of MOF and MARA

Publisher

MDPI AG

Subject

General Medicine

Reference39 articles.

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