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Mathematical modeling and analysis of in vitro actin filament dynamics and cell blebbing.

机译：体外肌动蛋白丝动力学和细胞起泡的数学建模和分析。

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摘要

The dynamics of the actin cytoskeleton are vital for cell motility observed in many biological processes, such as morphogenetic movements during embryotic development, fibroblast migration during wound healing, and chemotactic movements of immune cells. To fulfill specific tasks, motile cells manipulate various actin structures within regions such as the lamellipodium, filopodia and stress fibers. A large pool of regulatory proteins and motor molecules coordinate the dynamic change of these structures to generate mechanical forces.In this thesis, we first investigate the temporal evolution of filament length distribution in a deterministic approach. The change of filament lengths is described by ordinary differential equations, and effects of diverse regulatory mechanisms are explored. We predict that the endwise polymerization alone produces a long-lived Gaussian-like distribution of filament lengths, which eventually evolves to an exponential distribution. The introduction of fragmentation drastically leads to a Bessel-type equilibrium distribution. Our model confirms that profilin proteins slow filament growth, decreases the extent of polymerization, and promote filament treadmilling. Actin monomers are associated with nucleotide ATP. In a filament, ATP can hydrolyze randomly into ADP-Pi, and subsequently release the phoshpate becoming ADP. Random ATP hydrolysis complicates the filament dynamics. The effect is analyzed in a stochastic model where each subunit within a filament is distinguished by associated nucleotide types. We theoretically predict a large length fluctuation occurring around the critical concentration of ATP-actin where the filament tip is bound intermittently by nucleotides ADP and ATP. By implementing an efficient stochastic simulation algorithm, we are able to track the evolution of length and nucleotide profile of single filament.We also investigate the phenomenon of cell blebbing, a typical membrane protrusion driven by actin dynamics and acto-myosin contraction. The major components of blebbing cells are recognized, and models for each component and their interaction are individually considered. Our analysis shows that a simple constraint on the membrane expansion rate relates the dynamic bleb size with the ring constricting the bleb. The properties of equilibrium state of blebbing are probed in a mechanical model whereby a uniform hydrostatic pressure is established by the balance of membrane tension in the contracting and expanding cell domains. We recognize that a potential membrane flow is important in establishing the blebbing equilibrium, and the influence of various flow types is compared.
机译：肌动蛋白细胞骨架的动力学对于在许多生物学过程中观察到的细胞运动至关重要，例如胚胎发育过程中的形态发生运动，伤口愈合过程中的成纤维细胞迁移以及免疫细胞的趋化运动。为了完成特定任务，运动细胞操纵区域内的各种肌动蛋白结构，例如片状脂蛋白，丝状伪足和应激纤维。大量的调节蛋白和运动分子协调这些结构的动态变化以产生机械力。在本文中，我们首先以确定性方法研究了长丝长度分布的时间演变。细丝长度的变化由常微分方程描述，并探索了各种调节机制的影响。我们预测仅单向聚合会产生长寿命的长丝状高斯分布，最终会演变成指数分布。碎片的引入极大地导致了贝塞尔型平衡分布。我们的模型证实，profilin蛋白可减慢细丝的生长，降低聚合程度，并促进细丝的跑步。肌动蛋白单体与核苷酸ATP相关。在细丝中，ATP可以随机水解为ADP-Pi，然后释放出磷酸酯，成为ADP。随机ATP水解使灯丝动力学复杂化。在随机模型中分析效果，其中通过关联的核苷酸类型区分细丝中的每个亚基。从理论上讲，我们预测在临界浓度的ATP-肌动蛋白附近会发生较大的长度波动，在该浓度下，细丝尖端被核苷酸ADP和ATP间歇性结合。通过实施高效的随机模拟算法，我们能够跟踪单丝的长度和核苷酸谱的演变。我们还研究了细胞起泡现象，这是由肌动蛋白动力学和肌动蛋白-肌动蛋白收缩驱动的典型膜突出。识别起泡细胞的主要成分，并分别考虑每种成分的模型及其相互作用。我们的分析表明，对膜膨胀速率的简单限制将动态气泡大小与环限制了气泡相关。在机械模型中探究起泡的平衡状态的性质，从而通过收缩和扩展细胞域中的膜张力平衡来建立均匀的静水压力。我们认识到，潜在的膜流动对于建立起泡平衡很重要，并且比较了各种流动类型的影响。

著录项

  • 作者

    Hu, Jifeng.;

  • 作者单位

    University of Minnesota.;

  • 授予单位 University of Minnesota.;
  • 学科 Applied Mathematics.
  • 学位 Ph.D.
  • 年度 2009
  • 页码 172 p.
  • 总页数 172
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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