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首页> 外文期刊>Molecular and Cellular Biology >E2F-Dependent Histone Acetylation and Recruitment of the Tip60 Acetyltransferase Complex to Chromatin in Late G1
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E2F-Dependent Histone Acetylation and Recruitment of the Tip60 Acetyltransferase Complex to Chromatin in Late G1

机译：E2F依赖的组蛋白乙酰化和晚期G1的Tip60乙酰转移酶复合物对染色质的募集

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E2F proteins can either activate or repress transcription. Following mitogenic stimulation, repressive E2F4-p130-histone deacetylase complexes dissociate from, while activating species (E2F1, -2, and -3) associate with, target promoters. Histones H3 and H4 simultaneously become hyperacetylated, but it remains unclear whether this is a prerequisite or a consequence of E2F binding. Here, we show that activating E2F species are required for hyperacetylation of target chromatin in human cells. Overexpression of a dominant-negative (DN) E2F1 mutant in serum-stimulated T98G cells blocked all E2F binding, H4 acetylation, and, albeit partially, H3 acetylation. Target gene activation and S-phase entry were also blocked by DN E2F1. Conversely, ectopic activation of E2F1 rapidly induced H3 and H4 acetylation, demonstrating a direct role for E2F in these events. E2F1 was previously shown to bind the histone acetyltransferases (HATs) p300/CBP and PCAF/GCN5. In our hands, ectopically expressed E2F1 also bound the unrelated HAT Tip60 and induced recruitment of five subunits of the Tip60 complex (Tip60, TRRAP, p400, Tip48, and Tip49) to target promoters in vivo. Moreover, E2F-dependent recruitment of Tip60 to chromatin occurred in late G1 following serum stimulation. We speculate that the activities of multiple HAT complexes account for E2F-dependent acetylation, transcription, and S-phase entry.
机译：E2F蛋白可以激活或抑制转录。有丝分裂刺激后，抑制性E2F4-p130-组蛋白脱乙酰酶复合物从靶启动子上解离，而活化种（E2F1，-2和-3）与靶启动子结合。组蛋白H3和H4同时变为超乙酰化的，但尚不清楚这是否是E2F结合的先决条件或结果。在这里，我们表明激活E2F物种是人类细胞中目标染色质超乙酰化所必需的。在血清刺激的T98G细胞中显性阴性（DN）E2F1突变体的过表达阻止了所有E2F结合，H4乙酰化以及（尽管部分地）H3乙酰化。靶基因激活和S期进入也被DN E2F1阻断。相反，E2F1的异位激活迅速诱导H3和H4乙酰化，证明E2F在这些事件中具有直接作用。先前显示E2F1与组蛋白乙酰转移酶（HATs）p300 / CBP和PCAF / GCN5结合。在我们手中，异位表达的E2F1还与无关的HAT Tip60结合，并诱导了Tip60复合物的五个亚基（Tip60，TRRAP，p400，Tip48和Tip49）募集到体内靶向启动子。此外，血清刺激后的G 1 晚期发生了E2F依赖的Tip60向染色质的募集。我们推测多个HAT复合物的活动解释了E2F依赖的乙酰化，转录和S期进入。

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