What determines the folding of the chromatin fiber?
What determines the folding of the chromatin fiber?
复制标题
染色质纤维的折叠由什么决定？
DOI：
10.1073/pnas.93.20.10548
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发表时间：
1996
影响因子：
11.1
通讯作者：
Zlatanova,J
中科院分区：
文献类型：
--
作者：
vanHolde,K;Zlatanova,J
在这篇综述中，我们试图总结，在一个关键的方式，目前已知的染色质纤维的凝聚和去凝聚的过程。我们开始与凝聚的可能机制的批判性分析，考虑到新旧证据是否核小体之间的连接DNA弯曲或保持直的凝聚结构。得出结论，优势的证据是直链接，我们问什么其他的基本过程可能允许缩合，并认为有证据表明，连接组蛋白诱导收缩的核小体间角，作为盐浓度提高到生理水平。我们还想知道，即使在生理盐浓度下，染色质的某些特定区域是如何变得去致密以允许转录的。我们认为接头组蛋白耗尽和核心组蛋白尾部的乙酰化是可能的机制。在最近的证据的基础上，我们提出了一个统一的模型，连接特定基因组区域的靶向乙酰化连接组蛋白耗尽，从而展开凝聚的纤维。
In this review, we attempt to summarize, in a critical manner, what is currently known about the processes of condensation and decondensation of chromatin fibers. We begin with a critical analysis of the possible mechanisms for condensation, considering both old and new evidence as to whether the linker DNA between nucleosomes bends or remains straight in the condensed structure. Concluding that the preponderance of evidence is for straight linkers, we ask what other fundamental process might allow condensation, and argue that there is evidence for linker histone-induced contraction of the internucleosome angle, as salt concentration is raised toward physiological levels. We also ask how certain specific regions of chromatin can become decondensed, even at physiological salt concentration, to allow transcription. We consider linker histone depletion and acetylation of the core histone tails, as possible mechanisms. On the basis of recent evidence, we suggest a unified model linking targeted acetylation of specific genomic regions to linker histone depletion, with unfolding of the condensed fiber as a consequence.