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首页> 外文期刊>Cell cycle >Chromatin unfolding by Cdt1 regulates MCM loading via opposing functions of HBO1 and HDAC11-geminin.
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Chromatin unfolding by Cdt1 regulates MCM loading via opposing functions of HBO1 and HDAC11-geminin.

机译：Cdt1产生的染色质通过HBO1和HDAC11-geminin的相反功能调节MCM负载。

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摘要

The efficiency of metazoan origins of DNA replication is known to be enhanced by histone acetylation near origins. Although this correlates with increased MCM recruitment, the mechanism by which such acetylation regulates MCM loading is unknown. We show here that Cdt1 induces large-scale chromatin decondensation that is required for MCM recruitment. This process occurs in G, is suppressed by Geminin, and requires HBO1 HAT activity and histone H4 modifications. HDAC11, which binds Cdt1 and replication origins during S-phase, potently inhibits Cdt1-induced chromatin unfolding and re-replication, suppresses MCM loading and binds Cdt1 more efficiently in the presence of Geminin. We also demonstrate that chromatin at endogenous origins is more accessible in G relative to S-phase. These results provide evidence that histone acetylation promotes MCM loading via enhanced chromatin accessibility. This process is regulated positively by Cdt1 and HBO1 in G and repressed by Geminin-HDAC11 association with Cdt1 in S-phase, and represents a novel form of replication licensing control.
机译：已知通过复制附近的组蛋白乙酰化可以提高后代起源的DNA复制效率。尽管这与增加的MCM募集有关，但是这种乙酰化调节MCM负载的机制尚不清楚。我们在这里表明，Cdt1诱导大规模MCM招聘所需的染色质缩聚。此过程发生在G中，被Geminin抑制，需要HBO1 HAT活性和组蛋白H4修饰。 HDAC11在S期结合Cdt1和复制起点，有效抑制Cdt1诱导的染色质展开和再复制，抑制了MCM的加载，并在Geminin存在下更有效地结合了Cdt1。我们还证明，相对于S期，内源性的染色质在G中更易于访问。这些结果提供了组蛋白乙酰化通过增强的染色质可及性促进MCM加载的证据。此过程受G中Cdt1和HBO1的正调控，并被Geminin-HDAC11与S期Cdt1的缔合抑制，代表了复制许可控制的一种新形式。

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