Department of Chemistry and Biochemistry, Institute for Physical Science and Technology, Chemical Physics Program, University of Maryland, College Park, MD 20742, USA.
Proc Natl Acad Sci U S A. 2012 Oct 30;109(44):17857-62. doi: 10.1073/pnas.1201805109. Epub 2012 Sep 17.
Intrinsically disordered proteins (IDP) are a broad class of proteins with relatively flat energy landscapes showing a high level of functional promiscuity, which are frequently regulated through posttranslational covalent modifications. Histone tails, which are the terminal segments of the histone proteins, are prominent IDPs that are implicated in a variety of signaling processes, which control chromatin organization and dynamics. Although a large body of work has been done on elucidating the roles of posttranslational modifications in functional regulation of IDPs, molecular mechanisms behind the observed behaviors are not fully understood. Using extensive atomistic molecular dynamics simulations, we found in this work that H4 tail mono-acetylation at LYS-16, which is a key covalent modification, induces a significant reorganization of the tail's conformational landscape, inducing partial ordering and enhancing the propensity for alpha-helical segments. Furthermore, our calculations of the potentials of mean force between the H4 tail and a DNA fragment indicate that contrary to the expectations based on simple electrostatic reasoning, the Lys-16 mono-acetylated H4 tail binds to DNA stronger than the unacetylated protein. Based on these results, we propose a molecular mechanism for the way Lys-16 acetylation might lead to experimentally observed disruption of compact chromatin fibers.
无规则蛋白质(IDP)是一大类蛋白质,它们具有相对平坦的能量景观,表现出高度的功能混杂性,这些功能通常通过翻译后共价修饰来调节。组蛋白尾部是组蛋白蛋白的末端片段,是一种突出的 IDP,它参与了多种信号转导过程,这些过程控制着染色质的组织和动力学。尽管已经做了大量的工作来阐明翻译后修饰在 IDP 功能调节中的作用,但观察到的行为背后的分子机制尚不完全清楚。在这项工作中,我们使用广泛的原子分子动力学模拟发现,H4 尾部赖氨酸 16 的单乙酰化,这是一种关键的共价修饰,诱导尾部构象景观的显著重排,诱导部分有序并增强α-螺旋片段的倾向。此外,我们计算了 H4 尾部与 DNA 片段之间的平均力势能表明,与基于简单静电推理的预期相反,赖氨酸 16 单乙酰化的 H4 尾部与 DNA 的结合比未乙酰化的蛋白质更强。基于这些结果,我们提出了一种分子机制,说明赖氨酸 16 乙酰化如何导致实验观察到的紧凑染色质纤维的破坏。