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O-GlcNAcylation of Mef2c regulates myoblast differentiation

Authors
 Han Byeol Kim  ;  Hyeon Gyu Seo  ;  SeongJin Son  ;  Hyeonjin Choi  ;  Byung Gyu Kim  ;  Tae Hyun Kweon  ;  Sunghoon Kim  ;  Jaeyoung Pai  ;  Injae Shin  ;  Won Ho Yang  ;  Jin Won Cho 
Citation
 BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, Vol.529(3) : 692-698, 2020-08 
Journal Title
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
ISSN
 0006-291X 
Issue Date
2020-08
MeSH
Acetylglucosamine / metabolism* ; Acylation ; Animals ; Cell Differentiation* ; Cell Line ; Glycosylation ; HEK293 Cells ; Humans ; MEF2 Transcription Factors / metabolism ; Mice ; Muscle Development* ; Muscle, Skeletal / cytology ; Muscle, Skeletal / metabolism ; Myoblasts / cytology* ; Myoblasts / metabolism
Keywords
O-GlcNAc ; Myoblast differentiation ; Mef2c ; Myogenin
Abstract
Unlike other types of glycosylation, O-GlcNAcylation is a single glycosylation which occurs exclusively in the nucleus and cytosol. O-GlcNAcylation underlie metabolic diseases, including diabetes and obesity. Furthermore,O-GlcNAcylation affects different oncogenic processes such as osteoblast differentiation, adipogenesis and hematopoiesis. Emerging evidence suggests that skeletal muscle differentiation is also regulated by O-GlcNAcylation, but the detailed molecular mechanism has not been fully elucidated. In this study, we showed that hyper-O-GlcNAcylation reduced the expression of myogenin, a transcription factor critical for terminal muscle development, in C2C12 myoblasts differentiation by O-GlcNAcylation on Thr9 of myocyte-specific enhancer factor 2c. Furthermore, we showed that O-GlcNAcylation on Mef2c inhibited its DNA binding affinity to myogenin promoter. Taken together, we demonstrated that hyper-O-GlcNAcylation attenuates skeletal muscle differentiation by increased O-GlcNAcylation on Mef2c, which downregulates its DNA binding affinity.
Full Text
https://www.sciencedirect.com/science/article/pii/S0006291X20312328
DOI
10.1016/j.bbrc.2020.06.031
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Biochemistry and Molecular Biology (생화학-분자생물학교실) > 1. Journal Papers
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/190024
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