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平滑肌肌球蛋白丝在体外沿肌动蛋白丝滑行的速度的动力学基础。

The kinetics underlying the velocity of smooth muscle myosin filament sliding on actin filaments in vitro.

出版信息

J Biol Chem. 2014 Jul 25;289(30):21055-70. doi: 10.1074/jbc.M114.564740.

Abstract

Actin-myosin interactions are well studied using soluble myosin fragments, but little is known about effects of myosin filament structure on mechanochemistry. We stabilized unphosphorylated smooth muscle myosin (SMM) and phosphorylated smooth muscle myosin (pSMM) filaments against ATP-induced depolymerization using a cross-linker and attached fluorescent rhodamine (XL-Rh-SMM). Electron micrographs showed that these side polar filaments are very similar to unmodified filaments. They are ~0.63 μm long and contain ~176 molecules. Rate constants for ATP-induced dissociation and ADP release from acto-myosin for filaments and S1 heads were similar. Actin-activated ATPases of SMM and XL-Rh-SMM were similarly regulated. XL-Rh-pSMM filaments moved processively on F-actin that was bound to a PEG brush surface. ATP dependence of filament velocities was similar to that for solution ATPases at high [actin], suggesting that both processes are limited by the same kinetic step (weak to strong transition) and therefore are attachment- limited. This differs from actin sliding over myosin monomers, which is primarily detachment-limited. Fitting filament data to an attachment-limited model showed that approximately half of the heads are available to move the filament, consistent with a side polar structure. We suggest the low stiffness subfragment 2 (S2) domain remains unhindered during filament motion in our assay. Actin-bound negatively displaced heads will impart minimal drag force because of S2 buckling. Given the ADP release rate, the velocity, and the length of S2, these heads will detach from actin before slack is taken up into a backwardly displaced high stiffness position. This mechanism explains the lack of detachment- limited kinetics at physiological [ATP]. These findings address how nonlinear elasticity in assemblies of motors leads to efficient collective force generation.

摘要

肌球蛋白丝结构对机械化学的影响知之甚少,但肌球蛋白片段的可溶性研究很好地研究了肌球蛋白与肌动蛋白的相互作用。我们使用交联剂和附着的荧光罗丹明(XL-Rh-SMM)稳定了未磷酸化的平滑肌肌球蛋白(SMM)和磷酸化的平滑肌肌球蛋白(pSMM)丝,以防止它们在 ATP 诱导下解聚。电子显微镜照片显示,这些侧极性丝与未修饰的丝非常相似。它们长约 0.63 μm,包含约 176 个分子。肌动球蛋白丝和 S1 头部的 ATP 诱导解离和 ADP 释放的速率常数相似。SMM 和 XL-Rh-SMM 的肌动球蛋白激活 ATPase 受到类似的调节。XL-Rh-pSMM 丝在与 PEG 刷表面结合的 F-肌动蛋白上进行连续运动。在高 [肌动蛋白] 下,细丝速度的 ATP 依赖性与溶液 ATPase 相似,这表明这两个过程都受到相同的动力学步骤(弱到强转变)的限制,因此都是附着限制的。这与肌动蛋白在肌球蛋白单体上滑动不同,后者主要是脱离限制的。将细丝数据拟合到附着限制模型表明,大约有一半的头部可以移动细丝,这与侧极性结构一致。我们假设在我们的测定中,低刚性的亚基 2(S2)结构域在细丝运动过程中不受阻碍。由于 S2 的弯曲,结合肌动蛋白的负位移头部将施加最小的阻力。考虑到 ADP 释放速率、速度和 S2 的长度,在松弛被吸收到向后位移的高刚性位置之前,这些头部将从肌动蛋白上脱离。这种机制解释了在生理 [ATP] 下缺乏脱离限制动力学的原因。这些发现解决了在马达组装体中非线性弹性如何导致有效集体力的产生。

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