Nothnagel E A, Webb W W
J Cell Biol. 1982 Aug;94(2):444-54. doi: 10.1083/jcb.94.2.444.
Cytoplasmic streaming in characean algae is thought to be driven by interaction between stationary subcortical actin bundles and motile endoplasmic myosin. Implicit in this mechanism is a requirement for some form of coupling to transfer motive force from the moving myosin to the endoplasm. Three models of viscous coupling between myosin and endoplasm are presented here, and the hydrodynamic feasibility of each model is analyzed. The results show that individual myosinlike molecules moving along the actin bundles at reasonable velocities cannot exert enough viscous pull on the endoplasm to account for the observed streaming. Attachment of myosin to small spherical organelles improves viscous coupling to the endoplasm, but results for this model show that streaming can be generated only if the myosin-spheres move along the actin bundles in a virtual solid line at about twice the streaming velocity. In the third model, myosin is incorporated into a fibrous or membranous network or gel extending into the endoplasm. This network is pulled forward as the attached myosin slides along the actin bundles. Using network dimensions estimated from published micrographs of characean endoplasm, the results show that this system can easily generate the observed cytoplasmic streaming.
轮藻中的细胞质流动被认为是由固定的皮层下肌动蛋白束与可移动的内质肌球蛋白之间的相互作用驱动的。这一机制隐含着需要某种形式的耦合，以将动力从移动的肌球蛋白传递到内质。本文提出了三种肌球蛋白与内质之间粘性耦合的模型，并分析了每种模型的流体动力学可行性。结果表明，沿着肌动蛋白束以合理速度移动的单个类肌球蛋白分子对内质施加的粘性拉力不足以解释观察到的流动现象。肌球蛋白附着在小的球形细胞器上可改善与内质的粘性耦合，但该模型的结果表明，只有当肌球蛋白球沿着肌动蛋白束以大约两倍于流动速度的虚拟实线移动时，才能产生流动。在第三个模型中，肌球蛋白被整合到延伸到内质中的纤维状或膜状网络或凝胶中。随着附着的肌球蛋白沿着肌动蛋白束滑动，这个网络被向前拉动。利用从已发表的轮藻内质显微照片估计的网络尺寸，结果表明该系统能够轻松产生观察到的细胞质流动。
