Mechanisms of actin-based force generation, morphodynamics and motility of single cells

细胞在胚胎发育、伤口愈合或肿瘤转移过程中爬行。在许多细胞类型和运动的多个阶段，产生运动的力量是通过假足、板脂或神经元生长锥体等膜突起中的肌动蛋白细丝聚合而建立的。同样的过程也推动了细胞形态动力学。目前的项目研究肌动蛋白聚合如何产生导致细胞运动和形态动力学的力。力-速度-关系将在恒定力和位置相关的力的情况下用扫描力显微镜测量。我们还将监测逆行肌动蛋白流动的功能和行为。调控肌动蛋白细丝的成核和交联将揭示这些参数和网络连接程度对细胞边缘突起和力产生的力学性质的影响。所有的实验都将得到数学模型的支持，关于机构的假设将以数学模型的形式定量地表达出来。

Cells crawl during embryogenesis, wound healing or tumor metastasis. In many cell types and in many phases of motility, the force generating motion is established by the polymerization of actin filaments in membrane protrusions like pseudopodia, lamellipodia or growth cones of neurons. The same processes also drive cellular morphodynamics. The current project investigates how actin polymerization generates the force causing cell motion and morphodynamics. The force-velocity-relation will be measured with constant and position-dependent force using scanning force microscopy. We will also monitor function and behavior of retrograde actin flow. Modulating actin filament nucleation and cross-linking will reveal the impact of these parameters and of the degree of network connectivity on the mechanical properties of cell edge protrusion and force generation. All experiments will be supported by mathematical modeling, and hypotheses on mechanisms will be quantitatively formulated in terms of mathematical models.