Histone dynamics on the interleukin-2 gene in response to T-Cell activation
Histone dynamics on the interleukin-2 gene in response to T-Cell activation
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DOI：
10.1128/mcb.25.8.3209-3219.2005
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发表时间：
2005-04-01
影响因子：
5.3
通讯作者：
Shannon, MF
中科院分区：
文献类型：
--
作者：
Chen, XX;Wang, J;Shannon, MF
已经提出了几个模型的机制，染色质重塑跨哺乳动物细胞中的诱导基因的启动子。最常见的模型是共占据模型，其中组蛋白通过乙酰化或磷酸化修饰，核小体重塑，允许转录因子复合物的组装。使用染色质免疫沉淀，我们观察到一个明显的减少组蛋白乙酰化和磷酸化信号的诱导型白细胞介素-2和粒细胞-巨噬细胞集落刺激因子基因的近端启动子区域在响应T细胞活化。我们发现，这种明显的减少是由于组蛋白H3和H4蛋白的损失相应的核小体占用的启动子减少。这种组蛋白丢失是可逆的;它依赖于适当的激活信号和转录因子的持续存在，而不依赖于组蛋白的乙酰化状态。这些数据首次表明，组蛋白的蛋白质是从哺乳动物启动子转录激活后丢失，并支持激活依赖的拆卸和核小体的重新组装的模型。
Several models have been proposed for the mechanism of chromatin remodelling across the promoters of inducible genes in mammalian cells. The most commonly held model is one of cooccupation where histone proteins are modified by acetylation or phosphorylation and nucleosomes are remodelled, allowing the assembly of transcription factor complexes. Using chromatin immunoprecipitation, we observed an apparent decrease of histone acetylation and phosphorylation signals at the proximal promoter region of the inducible interleukin-2 and granulocyte-macrophage colony-stimulating factor genes in response to T-cell activation. We showed that this apparent decrease was due to a loss of histone H3 and H4 proteins corresponding to a decrease in nucleosome occupation of the promoter. This histone loss is reversible; it is dependent on the continual presence of appropriate activating signals and transcription factors and is not dependent on the acetylation status of the histone proteins. These data show for the first time that histone proteins are lost from a mammalian promoter upon activation of transcription and support a model of activation-dependent disassembly and reassembly of nucleosomes.