Chromodomain protein CDYL is required for transmission/restoration of repressive histone marks | Zendy

Yongqing Liu | Zendy; Shumeng Liu | Zendy; Shuai Yuan | Zendy; Huajing Yu | Zendy; Yu Zhang | Zendy; Xiaohan Yang | Zendy; Guojia Xie | Zendy; Zhe Chen | Zendy; Wanjin Li | Zendy; Bosen Xu | Zendy; Luyang Sun | Zendy; Yongfeng Shang | Zendy; Jing Liang | Zendy

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Chromodomain protein CDYL is required for transmission/restoration of repressive histone marks

Author(s) -

Yongqing Liu,

Shumeng Liu,

Shuai Yuan,

Huajing Yu,

Yu Zhang,

Xiaohan Yang,

Guojia Xie,

Zhe Chen,

Wanjin Li,

Bosen Xu,

Luyang Sun,

Yongfeng Shang,

Jing Liang

Publication year - 2017

Publication title -

journal of molecular cell biology

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 1.825

H-Index - 62

eISSN - 1674-2788

pISSN - 1759-4685

DOI - 10.1093/jmcb/mjx013

Subject(s) - chromodomain , histone h2a , biology , microbiology and biotechnology , histone , histone code , chromatin , heterochromatin protein 1 , epigenetics , histone methyltransferase , nucleosome , genetics , heterochromatin , helicase , dna , gene , rna

Faithful transmission or restoration of epigenetic information such as repressive histone modifications through generations is critical for the maintenance of cell identity. We report here that chromodomain Y-like protein (CDYL), a chromodomain-containing transcription corepressor, is physically associated with chromatin assembly factor 1 (CAF-1) and the replicative helicase MCM complex. We showed that CDYL bridges CAF-1 and MCM, facilitating histone transfer and deposition during DNA replication. We demonstrated that CDYL recruits histone-modifying enzymes G9a, SETDB1, and EZH2 to replication forks, leading to the addition of H3K9me2/3 and H3K27me2/3 on newly deposited histone H3. Significantly, depletion of CDYL impedes early S phase progression and sensitizes cells to DNA damage. Our data indicate that CDYL plays an important role in the transmission/restoration of repressive histone marks, thereby preserving the epigenetic landscape for the maintenance of cell identity.

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