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首页> 外文期刊>Molecular and Cellular Biology >Histone Dynamics on the Interleukin-2 Gene in Response to T-Cell Activation
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Histone Dynamics on the Interleukin-2 Gene in Response to T-Cell Activation

机译：T细胞活化对白细胞介素2基因的组蛋白动力学

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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.
机译：已经提出了几种用于哺乳动物细胞中可诱导基因启动子的染色质重塑机制的模型。最常见的模型是一种共存模型，其中组蛋白通过乙酰化或磷酸化修饰，核小体被重塑，从而实现转录因子复合物的组装。使用染色质免疫沉淀，我们观察到可诱导的白介素2和粒细胞巨噬细胞集落刺激因子基因响应T细胞活化的近端启动子区域的组蛋白乙酰化和磷酸化信号明显减少。我们表明，这种明显的下降是由于组蛋白H3和H4蛋白的丢失所致，其对应于启动子的核小体占用的减少。这种组蛋白损失是可逆的。它取决于适当的激活信号和转录因子的持续存在，而与组蛋白的乙酰化状态无关。这些数据首次表明，在转录激活后，组蛋白从哺乳动物启动子中丢失，并支持核小体的激活依赖性拆卸和重组模型。

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