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重塑因子和组蛋白片段介导的随机核小体解体。

Stochastic nucleosome disassembly mediated by remodelers and histone fragmentation.

机构信息

Department of Computational Medicine, University of California, Los Angeles, California 90095-1766, USA.

Department of Mathematics, University of California, Los Angeles, California 90095-1555, USA.

出版信息

J Chem Phys. 2023 Nov 28;159(20). doi: 10.1063/5.0165136.

Abstract

We construct and analyze monomeric and multimeric models of the stochastic disassembly of a single nucleosome. Our monomeric model predicts the time needed for a number of histone-DNA contacts to spontaneously break, leading to dissociation of a non-fragmented histone from DNA. The dissociation process can be facilitated by DNA binding proteins or processing molecular motors that compete with histones for histone-DNA contact sites. Eigenvalue analysis of the corresponding master equation allows us to evaluate histone detachment times under both spontaneous detachment and protein-facilitated processes. We find that competitive DNA binding of remodeling proteins can significantly reduce the typical detachment time but only if these remodelers have DNA-binding affinities comparable to those of histone-DNA contact sites. In the presence of processive motors, the histone detachment rate is shown to be proportional to the product of the histone single-bond dissociation constant and the speed of motor protein procession. Our simple intact-histone model is then extended to allow for multimeric nucleosome kinetics that reveal additional pathways of disassembly. In addition to a dependence of complete disassembly times on subunit-DNA contact energies, we show how histone subunit concentrations in bulk solutions can mediate the disassembly process by rescuing partially disassembled nucleosomes. Moreover, our kinetic model predicts that remodeler binding can also bias certain pathways of nucleosome disassembly, with higher remodeler binding rates favoring intact-histone detachment.

摘要

我们构建并分析了单个核小体随机解组装的单体和多聚体模型。我们的单体模型预测了许多组蛋白-DNA 相互作用自发断裂所需的时间,导致非片段化组蛋白从 DNA 上解离。DNA 结合蛋白或加工分子马达可以促进解离过程,这些蛋白或马达与组蛋白竞争组蛋白-DNA 结合位点。相应主方程的特征值分析使我们能够评估自发和蛋白促进过程下的组蛋白脱离时间。我们发现,重塑蛋白的竞争性 DNA 结合可以显著降低典型的脱离时间,但前提是这些重塑蛋白具有与组蛋白-DNA 结合位点相当的 DNA 结合亲和力。在有动力蛋白的情况下,组蛋白脱离速率被证明与组蛋白单键离解常数和动力蛋白蛋白进程速度的乘积成正比。然后,我们将简单的完整组蛋白模型扩展到允许进行多聚体核小体动力学研究,揭示了更多的组装解体途径。除了完全组装时间依赖于亚基-DNA 接触能外,我们还展示了在大量溶液中组蛋白亚基浓度如何通过挽救部分解组装的核小体来介导解组装过程。此外,我们的动力学模型还预测,重塑酶的结合也可以使核小体解组装的某些途径产生偏差,较高的重塑酶结合速率有利于完整组蛋白的脱离。

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