Bidone Tamara Carla, Tang Haosu, Vavylonis Dimitrios
Lehigh University, Bethlehem PA, USA.
Int Mech Eng Congress Expo. 2014;9. doi: 10.1115/IMECE2014-39006.
During fission yeast cytokinesis, actin filaments nucleated by cortical formin Cdc12 are captured by myosin motors bound to a band of cortical nodes. The myosin motors exert forces that pull nodes together into a contractile ring. Cross-linking interactions help align actin filaments and nodes into a single bundle. Mutations in the myosin motor domain and changes in the concentration of cross-linkers alpha-actinin and fimbrin alter the morphology of the condensing network, leading to clumps, rings or extended meshworks. How the contractile tension developing during ring formation depends on the interplay between network morphology, myosin motor activity, cross-linking and actin filament turnover remains to be elucidated. We addressed this question using a 3D computational model in which semiflexible actin filaments (represented as beads connected by springs) grow from formins, can be captured by myosin in neighboring nodes, and get cross-linked with one another through an attractive interaction. We identify regimes of tension generation between connected nodes under a wide set of conditions regarding myosin dynamics and strength of cross-linking between actin filaments. We find conditions that maximize circumferential tension, correlate them with network morphology and propose experiments to test these predictions. This work addresses "Morphogenesis of soft and living matter" using computational modeling to simulate cytokinetic ring assembly from the key molecular mechanisms of viscoelastic cross-linked actin networks that include active molecular motors.
在裂殖酵母胞质分裂过程中,由皮层formin蛋白Cdc12成核的肌动蛋白丝被结合到皮层节点带的肌球蛋白马达捕获。肌球蛋白马达施加力,将节点拉到一起形成收缩环。交联相互作用有助于将肌动蛋白丝和节点排列成单个束。肌球蛋白马达结构域的突变以及交联蛋白α-肌动蛋白和丝束蛋白浓度的变化会改变凝聚网络的形态,导致形成团块、环或延伸的网络。在环形成过程中产生的收缩张力如何依赖于网络形态、肌球蛋白马达活性、交联和肌动蛋白丝周转之间的相互作用仍有待阐明。我们使用一个三维计算模型来解决这个问题,在该模型中,半柔性肌动蛋白丝(表示为由弹簧连接的珠子)从formin蛋白生长,可以被相邻节点中的肌球蛋白捕获,并通过吸引相互作用相互交联。我们确定了在关于肌球蛋白动力学和肌动蛋白丝之间交联强度的广泛条件下,相连节点之间产生张力的机制。我们找到了使圆周张力最大化的条件,将它们与网络形态相关联,并提出实验来检验这些预测。这项工作使用计算建模来模拟从包括活性分子马达的粘弹性交联肌动蛋白网络的关键分子机制进行的胞质分裂环组装,从而解决了“软物质和生命物质的形态发生”问题。