首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >SWI/SNF-dependent long-range remodeling of yeast HIS3 chromatin
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SWI/SNF-dependent long-range remodeling of yeast HIS3 chromatin

机译:SWI / SNF依赖的酵母HIS3染色质的远程重塑

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Current models for the role of the SWI/SNF chromatin remodeling complex in gene regulation are focused on promoters, where the most obvious changes in chromatin structure occur. Here we present evidence that the SWI/SNF complex is involved in the remodeling of the chromatin structure of an entire gene in vivo. We compared the native chromatin structures of a small yeast plasmid containing the HIS3 gene purified from uninduced and induced cells. Relative to uninduced chromatin, induced chromatin displayed a large reduction in negative supercoiling, a large reduction in sedimentation rate, and increased accessibility to restriction enzymes with sites located both near and far from the HIS3 promoter. These observations indicate that the entire plasmid was remodeled as a result of induction. Loss of supercoiling required the presence of the SWI/SNF remodeling complex and the activator Gcn4p in vivo. The TATA boxes were not required, suggesting that remodeling was not the result of transcription. The induction-dependent loss of negative supercoiling was not apparent in cells, indicating that the supercoils were lost preferentially from induced chromatin during purification. Thus, induced HIS3 chromatin has a highly labile structure that is revealed as a result of purification. It is concluded that induction of HIS3 creates a domain of labile chromatin structure that extends far beyond the promoter to include the entire gene. We propose that the SWI/SNF complex is recruited to the HIS3 promoter by Gcn4p and then directs remodeling of a chromatin domain, with important implications for transcription.
机译:SWI / SNF染色质重塑复合体在基因调控中的作用的当前模型集中在启动子上,其中染色质结构发生最明显的变化。在这里,我们提供证据表明SWI / SNF复合体参与了体内整个基因染色质结构的重塑。我们比较了一个小的酵母质粒的天然染色质结构,该质粒含有从未诱导和诱导的细胞中纯化的HIS3基因。相对于未诱导的染色质,诱导的染色质显示出负超螺旋的大幅降低,沉降速率的大幅降低以及对限制性酶的可及性的提高,限制性酶的位点均位于HIS3启动子附近。这些观察结果表明,由于诱导,整个质粒被重塑。超螺旋的损失需要在体内存在SWI / SNF重塑复合物和激活剂Gcn4p。不需要TATA框,表明重塑不是转录的结果。负依赖性超螺旋的诱导依赖性损失在细胞中不明显,表明超螺旋在纯化过程中优先从诱导染色质丢失。因此,诱导的HIS3染色质具有高度不稳定的结构,该结构通过纯化被揭示。结论是,HIS3的诱导产生了不稳定的染色质结构域,该结构域延伸到启动子之外,包括整个基因。我们建议SWI / SNF复合体被Gcn4p募集到HIS3启动子,然后指导染色质结构域的重塑,对转录具有重要意义。

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