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肌球蛋白头部相互作用及其被 2'-脱氧-ADP 修饰的动力学。

Interacting myosin head dynamics and their modification by 2'-deoxy-ADP.

机构信息

Department of Bioengineering, School of Medicine, University of Washington, Seattle, Washington.

Department of Biosciences, University of Kent, Kent, United Kingdom.

出版信息

Biophys J. 2024 Nov 19;123(22):3997-4008. doi: 10.1016/j.bpj.2024.10.013. Epub 2024 Oct 22.

Abstract

The contraction of striated muscle is driven by cycling myosin motor proteins embedded within the thick filaments of sarcomeres. In addition to cross-bridge cycling with actin, these myosin proteins can enter an inactive, sequestered state in which the globular S1 heads rest along the thick filament surface and are inhibited from performing motor activities. Structurally, this state is called the interacting heads motif (IHM) and is a critical conformational state of myosin that regulates muscle contractility and energy expenditure. Structural perturbation of the sequestered state can pathologically disrupt IHM structure and the mechanical performance of muscle tissue. Thus, the IHM state has become a target for therapeutic intervention. An ATP analog called 2'-deoxy-ATP (dATP) is a potent myosin activator that destabilizes the IHM. Here, we use molecular dynamics simulations to study the molecular mechanisms by which dATP modifies the structure and dynamics of myosin in a sequestered state. Simulations of the IHM state containing ADP.Pi in both nucleotide binding pockets revealed dynamic motions of the blocked head-free head interface, light chain binding domain, and S2 in this "inactive" state of myosin. Replacement of ADP.Pi by dADP.Pi triggered a series of structural changes that increased heterogeneity among residue contact pairs at the blocked head-free head interface and a 14% decrease in the interaction energy at the interface. Dynamic changes to this interface were accompanied by dynamics in the light chain binding region. A comparative analysis of these dynamics predicted new structural sites that may affect IHM stability.

摘要

横纹肌的收缩是由嵌入肌节粗丝中的肌球蛋白马达蛋白的循环驱动的。除了与肌动蛋白的交联循环外,这些肌球蛋白蛋白还可以进入无活性的隔离状态,此时球状 S1 头部沿着粗丝表面休息,并被抑制进行马达活动。从结构上讲,这种状态称为相互作用头部模体(IHM),是调节肌肉收缩性和能量消耗的肌球蛋白的关键构象状态。隔离状态的结构干扰可能会病理性地破坏 IHM 结构和肌肉组织的机械性能。因此,IHM 状态已成为治疗干预的目标。一种称为 2'-脱氧-ATP(dATP)的 ATP 类似物是一种有效的肌球蛋白激活剂,可破坏 IHM。在这里,我们使用分子动力学模拟研究 dATP 修饰隔离状态下肌球蛋白结构和动力学的分子机制。在核苷酸结合口袋中都含有 ADP.Pi 的 IHM 状态的模拟揭示了在肌球蛋白的“非活性”状态下,被封锁的头-无头接口、轻链结合结构域和 S2 的动态运动。用 dADP.Pi 取代 ADP.Pi 触发了一系列结构变化,增加了被封锁的头-无头接口处残基接触对的异质性,并使接口处的相互作用能降低了 14%。该接口的动态变化伴随着轻链结合区域的动力学变化。对这些动力学的比较分析预测了可能影响 IHM 稳定性的新结构位点。

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