Nucleosome sliding via TBP DNA binding in vivo
Nucleosome sliding via TBP DNA binding in vivo
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DOI：
10.1016/s0092-8674(01)00490-1
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发表时间：
2001-09-21
期刊：
影响因子：
64.5
通讯作者：
Thanos, D
中科院分区：
文献类型：
--
作者：
Lomvardas, S;Thanos, D
在这里，我们发现，干扰素β启动子的核小体在体内响应病毒感染而滑动，从而暴露了先前掩盖的TATA盒和起始位点，这是转录激活的必要条件。我们的实验还表明，这种染色质重塑模式是一个两步反应。首先，增强体招募 SWI/SNF 染色质重塑复合物，该复合物修饰核小体以允许 TBP 结合。其次，TBP 结合诱导 DNA 弯曲，核小体滑动到新位置。其他 DNA 结合蛋白的实验表明，DNA 弯曲能力与核小体滑动之间存在很强的相关性，表明滑动是由弯曲引起的。
Here, we show that a nucleosome obstructing transcription from the IFN-beta promoter slides in vivo in response to virus infection, thus exposing the previously masked TATA box and the initiation site, a requirement for transcriptional activation. Our experiments also revealed that this mode of chromatin remodeling is a two-step reaction. First, the enhanceosome recruits the SWI/SNF chromatin-remodeling complex that modifies the nucleosome to allow binding of TBP. Second, DNA bending is induced by TBP binding, and the nucleosome slides to a new position. Experiments with other DNA binding proteins demonstrated a strong correlation between the ability to bend DNA and nucleosome sliding, suggesting that the sliding is induced by the bend.