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染色质结合蛋白如何引导四核小体的不同折叠途径:来自粗粒度模拟的见解。

How chromatin-binding proteins direct distinct folding pathways of tetra-nucleosomes: Insights from coarse-grained simulations.

作者信息

Kapoor Utkarsh

机构信息

Department of Chemical and Biomedical Engineering, University of Wyoming, Laramie, WY 82071, United States.

出版信息

bioRxiv. 2025 Jul 31:2025.07.27.667063. doi: 10.1101/2025.07.27.667063.

Abstract

The dynamic coupling between chromatin organization and biomolecular condensates is governed by chromatin-binding proteins, yet the structural mechanisms by which these proteins modulate nucleosome interactions across spatial and organizational scales remain poorly understood. In this work, using high-resolution sequence-specific coarse-grained models combined with well-tempered metadynamics and parallel tempering, we investigate how heterochromatin protein 1α (HP1α) and a truncated construct of Polyhomeotic-like protein (tPHC3) influence the stability and folding pathways of tetra-nucleosomes, a minimal yet functionally informative chromatin model, under dilute and dense-phase conditions. While these proteins are known to drive distinct nuclear condensates their differential impact on chromatin topology and folding dynamics remains unclear. To address this, we ask: Do HP1α and tPHC3 stabilize or disrupt the canonical β-rhombus and α-tetrahedron nucleosome conformations? Are α-tetrahedron motifs transient intermediates or metastable states, and how do their prevalence and persistence depend on protein identity and phase context? To answer these questions, we analyze folding free energy landscapes, diffusion maps-based dimensionality reduced coordinates, and intermolecular interaction networks. Our simulations reveal that HP1α promote flexible, short-range nucleosome bridging and transient α-tetrahedron-like intermediates without stabilizing persistent structural basins. In contrast, tPHC3 stabilize α-tetrahedron-like motifs that scaffold folding toward the compact β-rhombus configuration characteristic of crystal-state tetra-nucleosomes. We find that this behavior arises from a context-dependent reorganization of multivalent SAM-linker interactions: in the absence of chromatin, self-association in dense phase conditions is mediated by linker-linker and linker-SAM contacts, while in the presence of nucleosomes, these linker-mediated interactions are suppressed, prompting compensatory SAM-SAM assembly. This reorganization highlights the essential role of SAM-mediated bridging in enabling long-range chromatin compaction. Together, our results demonstrate that under dense phase conditions α-tetrahedron-like motifs act as metastable intermediates rather than obligate folding end states, and their emergence depends critically on the identity of the chromatin-binding protein and their ability to mediate bridging. These insights offer a mechanistic framework for understanding how distinct architectural proteins encode topological preferences and remodel chromatin architecture across scales to support condensate formation and nuclear compartmentalization.

摘要

染色质组织与生物分子凝聚物之间的动态耦合由染色质结合蛋白控制,然而这些蛋白在空间和组织尺度上调节核小体相互作用的结构机制仍知之甚少。在这项工作中,我们使用高分辨率序列特异性粗粒度模型,并结合温和元动力学和平行回火,研究了异染色质蛋白1α(HP1α)和多同源样蛋白的截短构建体(tPHC3)在稀相和浓相条件下如何影响四核小体的稳定性和折叠途径,四核小体是一个最小但功能丰富的染色质模型。虽然已知这些蛋白会驱动不同的核凝聚物,但它们对染色质拓扑结构和折叠动力学的不同影响仍不清楚。为了解决这个问题,我们提出:HP1α和tPHC3是稳定还是破坏经典的β-菱形和α-四面体核小体构象?α-四面体基序是瞬态中间体还是亚稳态,它们的发生率和持久性如何取决于蛋白质身份和相环境?为了回答这些问题,我们分析了折叠自由能景观、基于扩散映射的降维坐标和分子间相互作用网络。我们的模拟表明,HP1α促进灵活的短程核小体桥接和瞬态α-四面体样中间体的形成,而不会稳定持久的结构盆地。相比之下,tPHC3稳定α-四面体样基序,这些基序支架折叠成晶体态四核小体特有的紧凑β-菱形构型。我们发现这种行为源于多价SAM-连接子相互作用的上下文依赖性重组:在没有染色质的情况下,浓相条件下的自缔合由连接子-连接子和连接子-SAM接触介导,而在有核小体的情况下,这些连接子介导的相互作用受到抑制,促使补偿性SAM-SAM组装。这种重组突出了SAM介导的桥接在实现长程染色质压实中的重要作用。总之,我们的结果表明,在浓相条件下,α-四面体样基序作为亚稳态中间体而非必然的折叠终态,它们的出现关键取决于染色质结合蛋白的身份及其介导桥接的能力。这些见解为理解不同的结构蛋白如何编码拓扑偏好并跨尺度重塑染色质结构以支持凝聚物形成和细胞核区室化提供了一个机制框架。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b6d/12324292/662942c0aee8/nihpp-2025.07.27.667063v1-f0001.jpg

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