Ph.D. Program in Biochemistry, The Graduate Center of the City University of New York, New York, New York 10016, United States.
Department of Chemistry, College of Staten Island, The City University of New York, 2800 Victory Boulevard, Staten Island, New York, New York 10314, United States.
J Chem Inf Model. 2024 Jun 24;64(12):4709-4726. doi: 10.1021/acs.jcim.4c00059. Epub 2024 Jun 12.
Epigenetic modifications of histone N-terminal tails play a critical role in regulating the chromatin structure and biological processes such as transcription and DNA repair. One of the key post-translational modifications (PTMs) is the acetylation of lysine residues on histone tails. Epigenetic modifications are ubiquitous in the development of diseases, such as cancer and neurological disorders. Histone H2B tails are critical regulators of nucleosome dynamics, biological processes, and certain diseases. Here, we report all-atomistic molecular dynamics (MD) simulations of the nucleosome to demonstrate that acetylation of the histone tails changes their conformational space and interaction with DNA. We perform simulations of H2B tails, critical regulators of gene regulation, in both the lysine-acetylated (ACK) and unacetylated wild type (WT) states. To explore the effects of salt concentration, we use two different NaCl concentrations to perform simulations at microsecond time scales. Salt can modulate the effects of electrostatic interactions between the DNA phosphate backbone and histone tails. Upon acetylation, H2B tails shift their secondary structure helical propensity. The number of contacts between the DNA and the H2B tail decreases. We characterize the conformational dynamics of the H2B tails by principal component analysis (PCA). The ACK tails become more compact at increased salt concentrations, but conformations from the WT tails display the most contacts with DNA at both salt concentrations. Mainly, H2B acetylation may increase the DNA accessibility for regulatory proteins to bind, which can aid in gene regulation and NCP stability.
组蛋白 N 端尾部的表观遗传修饰在调节染色质结构和转录、DNA 修复等生物过程中起着关键作用。其中一种关键的翻译后修饰(PTM)是赖氨酸残基在组蛋白尾部的乙酰化。表观遗传修饰在疾病的发展中普遍存在,如癌症和神经紊乱。组蛋白 H2B 尾部是核小体动力学、生物过程和某些疾病的关键调节因子。在这里,我们报告了核小体的全原子分子动力学(MD)模拟,以证明组蛋白尾部的乙酰化改变了它们的构象空间和与 DNA 的相互作用。我们模拟了组蛋白 H2B 尾部,它是基因调控的关键调节因子,分别在赖氨酸乙酰化(ACK)和未乙酰化野生型(WT)状态下进行模拟。为了探索盐浓度的影响,我们使用两种不同的 NaCl 浓度在微秒时间尺度上进行模拟。盐可以调节 DNA 磷酸骨架和组蛋白尾部之间的静电相互作用的影响。乙酰化后,H2B 尾部改变其二级结构螺旋倾向。DNA 与 H2B 尾部之间的接触数量减少。我们通过主成分分析(PCA)来描述 H2B 尾部的构象动力学。ACK 尾部在增加盐浓度时变得更加紧凑,但 WT 尾部的构象在两种盐浓度下都与 DNA 有最多的接触。主要的是,H2B 乙酰化可能增加了调节蛋白与 DNA 结合的可及性,这有助于基因调控和 NCP 的稳定性。