ZMYND8 Reads the Dual Histone Mark H3K4me1-H3K14ac to Antagonize the Expression of Metastasis-Linked Genes

被引：107

作者：

Li, Na ^{[1
]}

Li, Yuanyuan ^{[2
,3
]}

Lv, Jie ^{[4
,5
,6
]}

Zheng, Xiangdong ^{[2
,3
]}

Wen, Hong ^{[7
]}

Shen, Hongjie ^{[8
,9
]}

Zhu, Guangjing ^{[10
]}

Chen, Tsai-Yu ^{[1
]}

Dhar, Shilpa S. ^{[1
]}

Kan, Pu-Yeh ^{[1
]}

Wang, Zhibin ^{[10
]}

Shiekhattar, Ramin ^{[11
]}

Shi, Xiaobing ^{[7
]}

Lan, Fei ^{[8
,9
]}

Chen, Kaifu ^{[4
,5
,6
]}

Li, Wei ^{[12
,13
]}

Li, Haitao ^{[2
,3
,14
]}

Lee, Min Gyu ^{[1
,15
]}

机构：

[1] Univ Texas MD Anderson Canc Ctr, Dept Mol & Cellular Oncol, 1515 Holcombe Blvd, Houston, TX 77030 USA

[2] Tsinghua Univ, Dept Basic Med Sci, Beijing Adv Innovat Ctr Struct Biol, MOE Key Lab Prot Sci,Sch Med, Beijing 100084, Peoples R China

[3] Tsinghua Univ, Tsinghua Peking Ctr Life Sci, Beijing 100084, Peoples R China

[4] Methodist Hosp, Res Inst, Inst Acad Med, Houston, TX 77030 USA

[5] Methodist Hosp, Dept Cardiovasc Sci, Ctr Cardiovasc Regenerat, Res Inst, Houston, TX 77030 USA

[6] Cornell Univ, Weill Cornell Med Coll, New York, NY 10065 USA

[7] Univ Texas MD Anderson Canc Ctr, Dept Epigenet & Mol Carcinogenesis, 1515 Holcombe Blvd, Houston, TX 77030 USA

[8] Fudan Univ, Inst Biomed Sci, Key Lab Epigenet, Childrens Hosp, Shanghai 201102, Peoples R China

[9] Fudan Univ, Childrens Hosp, Key Lab Birth Defect, Shanghai 201102, Peoples R China

[10] Johns Hopkins Univ, Bloomberg Sch Publ Hlth, Dept Environm Hlth Sci, Baltimore, MD 21205 USA

[11] Univ Miami, Miller Sch Med, Sylvester Comprehens Canc Ctr, Dept Human Genet, Biomed Res Bldg,1501 NW 10th Ave, Miami, FL 33136 USA

[12] Baylor Coll Med, Dan L Duncan Canc Ctr, Div Biostat, One Baylor Plaza, Houston, TX 77030 USA

[13] Baylor Coll Med, Dept Mol & Cellular Biol, One Baylor Plaza, Houston, TX 77030 USA

[14] Sichuan Univ, West China Hosp, Collaborat Innovat Ctr Biotherapy, Chengdu 610041, Peoples R China

[15] Univ Texas Grad Sch Biomed Sci Houston, Canc Biol Program, Houston, TX 77030 USA

来源：

MOLECULAR CELL | 2016年 / 63卷 / 03期

基金：

中国国家自然科学基金; 中国博士后科学基金;

关键词：

TUMOR-METASTASIS; HUMAN GENOME; DNA-DAMAGE; STEM-CELLS; TANDEM PHD; METHYLATION; CANCER; H3; TRANSCRIPTION; ACETYLATION;

D O I：

10.1016/j.molcel.2016.06.035

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Histone acetylation, including acetylated H3K14 (H3K14ac), is generally linked to gene activation. Monomethylated histone H3 lysine 4 (H3K4me1), together with other gene-activating marks, denotes active genes. In contrast to usual gene-activating functions of H3K14ac and H3K4me1, we here show that the dual histone modification mark H3K4me1-H3K14ac is recognized by ZMYND8 (also called RACK7) and can function to counteract gene expression. We identified ZMYND8 as a transcriptional corepressor of the H3K4 demethylase JARID1D. ZMYND8 antagonized the expression of metastasis-linked genes, and its knockdown increased the cellular invasiveness in vitro and in vivo. The plant homeodomain (PHD) and Bromodomain cassette in ZMYND8 mediated the combinatorial recognition of H3K4me1-H3K14ac and H3K4me0-H3K14ac by ZMYND8. These findings uncover an unexpected role for the signature H3K4me1-H3K14ac in attenuating gene expression and reveal a metastasis-suppressive epigenetic mechanism in which ZMYND8's PHD-Bromo cassette couples H3K4me1-H3K14ac with downregulation of metastasis-linked genes.

引用

页码：470 / 484

页数：15

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