KAT5-mediated SOX4 acetylation orchestrates chromatin remodeling during myoblast differentiation

被引：26

作者：

Jang, S-M ^{[1
]}

Kim, J-W ^{[1
]}

Kim, C-H ^{[1
]}

An, J-H ^{[1
]}

Johnson, A. ^{[2
]}

Song, P. I. ^{[3
]}

Rhee, S. ^{[1
]}

Choi, K-H ^{[1
]}

机构：

[1] Chung Ang Univ, Dept Life Sci, Seoul 156756, South Korea

[2] Univ Arkansas Med Sci, Dept Dermatol, Little Rock, AR 72205 USA

[3] Univ Colorado Denver, Dept Dermatol, Aurora, CO 80045 USA

来源：

CELL DEATH & DISEASE | 2015年 / 6卷

基金：

新加坡国家研究基金会;

关键词：

HISTONE ACETYLTRANSFERASE TIP60; SKELETAL-MUSCLE DIFFERENTIATION; TRANSCRIPTIONAL ACTIVITY; GENE-EXPRESSION; EPIGENETIC REGULATION; RETINA DEVELOPMENT; MYST FAMILY; DNA-DAMAGE; STEM-CELLS; MYOD;

D O I：

10.1038/cddis.2015.190

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

Transcription factor SOX4 has been implicated in skeletal myoblast differentiation through the regulation of Cald1 gene expression; however, the detailed molecular mechanism underlying this process is largely unknown. Here, we demonstrate that SOX4 acetylation at lysine 95 by KAT5 (also known as Tip60) is essential for Cald1 promoter activity at the onset of C2C12 myoblast differentiation. KAT5 chromodomain was found to facilitate SOX4 recruitment to the Cald1 promoter, which is involved in chromatin remodeling at the promoter. Chromatin occupancy analysis of SOX4, KAT5, and HDAC1 indicated that the expression of putative SOX4 target genes during C2C12 myoblast differentiation is specifically regulated by the molecular switching of the co-activator KAT5 and the co-repressor HDAC1 on SOX4 transcriptional activation.

引用

页码：e1857 / e1857

页数：11

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