Models for actin polymerization motors
Models for actin polymerization motors
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DOI：
10.1007/s00285-008-0200-4
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发表时间：
2009-01-01
影响因子：
1.9
通讯作者：
Dickinson, Richard B.
中科院分区：
文献类型：
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作者：
Dickinson, Richard B.
肌动蛋白聚合驱动细胞膜突起和细胞内病原体的推进。驱动肌动蛋白聚合的分子机制尚未完全了解。已经提出了各种数学模型来解释细胞如何将肌动蛋白聚合时释放的化学能转化为表面上的推力。这些模型试图解释肌动蛋白为基础的运动性，包括持续附着的网络推进过程中的膜和推进粒子的有趣的轨迹令人费解的属性。这些模型通常分为两类：需要细丝（+）-末端从膜上自由波动以添加亚基的模型，以及细丝伸长且其（+）-末端持续与表面通过细丝末端跟踪蛋白相关联的模型（“actoclampin”模型）。这篇评论比较和对比这两类模型的力-速度曲线的关键预测，并评估它们与仿生粒子的实验，以及末端跟踪蛋白质，如formins和成核促进因子在肌动蛋白为基础的运动中的作用的实验证据。
Actin polymerization drives cell membrane protrusions and the propulsion of intracellular pathogens. The molecular mechanisms driving actin polymerization are not yet fully understood. Various mathematical models have been proposed to explain how cells convert chemical energy released upon actin polymerization into a pushing force on a surface. These models have attempted to explain puzzling properties of actin-based motility, including persistent attachment of the network to the membrane during propulsion and the interesting trajectories of propelled particles. These models fall generally into two classes: those requiring filament (+)-ends to fluctuate freely from the membrane to add subunits, and those where filaments elongate with their (+)-ends persistently associated with surface through filament end-tracking proteins ("actoclampin" models). This review compares and contrasts the key predictions of these two classes of models with regard to force-velocity profiles, and evaluates them with respect to experiments with biomimetic particles, and the experimental evidence on the role of end-tracking proteins such as formins and nucleation-promoting factors in actin-based motility.