Department of Biology, University of West Georgia, Carrollton, Georgia, United States of America.
PLoS One. 2009 Dec 8;4(12):e8052. doi: 10.1371/journal.pone.0008052.
Cooperative activation of striated muscle by calcium is based on the movement of tropomyosin described by the steric blocking theory of muscle contraction. Presently, the Hill model stands alone in reproducing both myosin binding data and a sigmoidal-shaped curve characteristic of calcium activation (Hill TL (1983) Two elementary models for the regulation of skeletal muscle contraction by calcium. Biophys J 44: 383-396.). However, the free myosin is assumed to be fixed by the muscle lattice and the cooperative mechanism is based on calcium-dependent interactions between nearest neighbor tropomyosin subunits, which has yet to be validated. As a result, no comprehensive model has been shown capable of fitting actual tension data from striated muscle. We show how variable free myosin is a selective advantage for activating the muscle and describe a mechanism by which a conformational change in tropomyosin propagates free myosin given constant total myosin. This mechanism requires actin, tropomyosin, and filamentous myosin but is independent of troponin. Hence, it will work equally well with striated, smooth and non-muscle contractile systems. Results of simulations with and without data are consistent with a strand of tropomyosin composed of approximately 20 subunits being moved by the concerted action of 3-5 myosin heads, which compares favorably with the predicted length of tropomyosin in the overlap region of thick and thin filaments. We demonstrate that our model fits both equilibrium myosin binding data and steady-state calcium-dependent tension data and show how both the steepness of the response and the sensitivity to calcium can be regulated by the actin-troponin interaction. The model simulates non-cooperative calcium binding both in the presence and absence of strong binding myosin as has been observed. Thus, a comprehensive model based on three well-described interactions with actin, namely, actin-troponin, actin-tropomyosin, and actin-myosin can explain the cooperative calcium activation of striated muscle.
肌球蛋白结合数据和钙激活的 S 形曲线特征(Hill TL(1983)两种用于调节骨骼肌收缩的基本模型钙。生物物理杂志 44:383-396。)。然而,自由肌球蛋白被假设为由肌肉晶格固定,协同机制基于钙依赖性相邻 tropomyosin 亚基之间的相互作用,这尚未得到验证。因此,没有综合模型能够拟合来自横纹肌的实际张力数据。我们展示了可变的自由肌球蛋白如何成为激活肌肉的优势,并描述了一种在恒定总肌球蛋白的情况下,tropomyosin 构象变化传播自由肌球蛋白的机制。这种机制需要肌动蛋白、tropomyosin 和丝状肌球蛋白,但不依赖肌钙蛋白。因此,它将与横纹肌、平滑肌和非肌肉收缩系统同样有效。有数据和没有数据的模拟结果一致,表明由大约 20 个亚基组成的 tropomyosin 链可以由 3-5 个肌球蛋白头部的协同作用移动,这与厚和薄丝重叠区域中 tropomyosin 的预测长度相当。我们证明了我们的模型既适合平衡肌球蛋白结合数据,也适合稳态钙依赖性张力数据,并展示了如何通过肌动蛋白-肌钙蛋白相互作用调节响应的陡峭程度和对钙的敏感性。该模型模拟了存在和不存在强结合肌球蛋白时非协同钙结合,这与观察到的情况一致。因此,基于与肌动蛋白的三种描述良好的相互作用(即肌动蛋白-肌钙蛋白、肌动蛋白-tropomyosin 和肌动蛋白-肌球蛋白)的综合模型可以解释横纹肌的协同钙激活。