HDAC11 inhibits myoblast differentiation through repression of MyoD-dependent transcription

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Title
HDAC11 inhibits myoblast differentiation through repression of MyoD-dependent transcription
Author(s)
Sang Kyung Byun; Tae Hyeon An; Min Jeong Son; Da Som Lee; Hyun Sup Kang; Eun Woo LeeBaek Soo HanWon Kon KimKwang-Hee BaeKyoung-Jin OhSang Chul Lee
Bibliographic Citation
Molecules and Cells, vol. 40, no. 9, pp. 667-676
Publication Year
2017
Abstract
Abnormal differentiation of muscle is closely associated with aging (sarcopenia) and diseases such as cancer and type II diabetes. Thus, understanding the mechanisms that regulate muscle differentiation will be useful in the treatment and prevention of these conditions. Protein lysine acetylation and methylation are major post-translational modification mechanisms that regulate key cellular processes. In this study, to elucidate the relationship between myogenic differentiation and protein lysine acetylation/methylation, we performed a PCR array of enzymes related to protein lysine acetylation/methylation during C2C12 myoblast differentiation. Our results indicated that the expression pattern of HDAC11 was substantially increased during myoblast differentiation. Furthermore, ectopic expression of HDAC11 completely inhibited myoblast differentiation, concomitant with reduced expression of key myogenic transcription factors. However, the catalytically inactive mutant of HDAC11 (H142/143A) did not impede myoblast differentiation. In addition, wild-type HDAC11, but not the inactive HDAC11 mutant, suppressed MyoD-induced promoter activities of MEF2C and MYOG (Myogenin), and reduced histone acetylation near the E-boxes, the MyoD binding site, of the MEF2C and MYOG promoters. Collectively, our results indicate that HDAC11 would suppress myoblast differentiation via regulation of MyoD-dependent transcription. These findings suggest that HDAC11 is a novel critical target for controlling myoblast differentiation.
Keyword
HDAC11lysine acetylationmyoblast differentiationMyoD-dependent transcription
ISSN
1016-8478
Publisher
South Korea
DOI
http://dx.doi.org/10.14348/molcells.2017.0116
Type
Article
Appears in Collections:
Division of Biomedical Research > Metabolic Regulation Research Center > 1. Journal Articles
Division of Research on National Challenges > Biodefense Research Center > 1. Journal Articles
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