ASF1A and ATM regulate H3K56-mediated cell-cycle checkpoint recovery in response to UV irradiation.
ASF1A and ATM regulate H3K56-mediated cell-cycle checkpoint recovery in response to UV irradiation.
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ASF1A和ATM调节H3K56介导的细胞周期检查点响应紫外线照射。
DOI：
10.1093/nar/gkr523
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发表时间：
2011-10
影响因子：
14.9
通讯作者：
Wani AA
中科院分区：
文献类型：
--
作者：
Battu A;Ray A;Wani AA
染色质内成功的 DNA 修复需要组蛋白修饰、分子伴侣和重塑剂之间的协调相互作用，以允许修复和检查点机器到达受损位点。修复完成后，染色质结构和关键表观遗传标记的有序恢复预示着细胞的正常功能。在这里，我们证明了 H3K56 乙酰化 (H3K56Ac) 标记响应人体细胞紫外线 (UV) 照射的恢复作用。 H3K56 快速初始脱乙酰化，随后在照射后约 24-48 小时完全更新乙酰化状态。组蛋白伴侣，抗沉默功能-1 A (ASF1A)，对于修复后 H3K56Ac 的恢复至关重要，而这又是 γ-H2AX 去磷酸化和细胞从检查点停滞中恢复所必需的。另一方面，DNA损伤修复的完成并不依赖于ASF1A或H3K56Ac。 H3K56Ac 恢复受共济失调毛细血管扩张突变 (ATM) 检查点激酶的调节。这些串扰分子细胞事件揭示了影响 H3K56Ac 在从紫外线诱导的检查点停滞恢复中的调节功能的重要途径成分。
Successful DNA repair within chromatin requires coordinated interplay of histone modifications, chaperones and remodelers for allowing access of repair and checkpoint machineries to damaged sites. Upon completion of repair, ordered restoration of chromatin structure and key epigenetic marks herald the cell’s normal function. Here, we demonstrate such a restoration role of H3K56 acetylation (H3K56Ac) mark in response to ultraviolet (UV) irradiation of human cells. A fast initial deacetylation of H3K56 is followed by full renewal of an acetylated state at ~24–48 h post-irradiation. Histone chaperone, anti-silencing function-1 A (ASF1A), is crucial for post-repair H3K56Ac restoration, which in turn, is needed for the dephosphorylation of γ-H2AX and cellular recovery from checkpoint arrest. On the other hand, completion of DNA damage repair is not dependent on ASF1A or H3K56Ac. H3K56Ac restoration is regulated by ataxia telangiectasia mutated (ATM) checkpoint kinase. These cross-talking molecular cellular events reveal the important pathway components influencing the regulatory function of H3K56Ac in the recovery from UV-induced checkpoint arrest.
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DOI：
10.1126/science.1135862
发表时间：
2007-02-02
期刊：
Science (New York, N.Y.)
影响因子：
--
作者：
Driscoll R;Hudson A;Jackson SP
通讯作者：
Jackson SP
影响因子：
13.8
作者：
Das, Chandrima;Tyler, Jessica K.;Churchill, Mair E. A.
通讯作者：
Churchill, Mair E. A.
影响因子：
11.4
作者：
Brand, M;Moggs, JG;Tora, L
通讯作者：
Tora, L
影响因子：
3.1
作者：
Ishikawa, Kazuhiro;Ishii, Hideshi;Saito, Toshiyuki
通讯作者：
Saito, Toshiyuki
影响因子：
10.5
作者：
Hu, FH;Alcasabas, AA;Elledge, SJ
通讯作者：
Elledge, SJ