O-GlcNAcylation of Mef2c regulates myoblast differentiation.

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. Copyright © 2020 Elsevier Inc. All rights reserved.

Citation

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. O-GlcNAcylation of Mef2c regulates myoblast differentiation. Biochemical and biophysical research communications. 2020 Aug 27;529(3):692-698

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PMID: 32736694

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