群体细胞表界面形貌演化在胚胎发育、伤口愈合与肿瘤侵袭等重要生命过程中扮演关键角色，其涉及细胞间相互作用、细胞活性与力学约束等多因素耦合调控。深入理解群体细胞表界面形貌的时空演化行为，对于揭示生物组织的结构--功能关联及相关疾病的发生机制具有重要意义。本文结合细胞实验、理论建模与数值模拟，研究了群体细胞表界面的形貌动力学演化规律：首先，研究了混合体系中细胞分选产生的组织界面的形貌动力学。通过动力学分析，发现了沿界面传递的变形波，揭示了细胞活性在调控界面形态动力学和驱动波沿界面传播中的作用。基于色散关系，明确了活性介导的界面失稳和相干流是产生界面变形波的根源。分析了拓扑缺陷与界面的相互作用以及拓扑缺陷的空间分布特性。基于活性液晶模型，进一步阐释了组织界面波动的产生机制。其次，研究了群体细胞相变对组织表界面形成、演化及相动力学的影响。发现了脉冲激光调控的笼式相变，实现在非典型条件下群体细胞的动力学相变。研究了该相变过程的可逆性及相动力学性质，给出了动力学--拓扑学约束关系。发现相变诱导形成的流固耦合界面对细胞运动与能量分布具有明显调控作用。采用变形多边形的理论模型，复现了相变驱动下的动力学与拓扑演化，展示了其作为空间可调、非接触式界面形态控制策略的前景。最后，对三维组织表面的形貌动力学进行研究。发展了基于胶原凝胶的三维组织表面实验系统，分析了多个细胞系的三维群体运动行为与团簇表面演化特征。描述了群体细胞运动模式及模式转换对团簇表面形貌演化的影响。引入整体拓扑性质的描述，揭示了团簇中囊腔结构的形成、融合与拓扑转变机制。综上所述，本文围绕群体细胞表界面的动力学过程，构建了多尺度、多方法融合的研究框架，揭示了组织表界面复杂形貌演化的机制。研究结果深化了对细胞群体动力学与组织表界面演化的认识，也为表界面功能调控与生物组织工程的理论建构提供了新思路与实验支撑。
The morphodynamic evolution of collective cellular surfaces and interfaces plays a pivotal role in essential biological processes such as embryonic development, wound healing, and tumor invasion. This evolution arises from the coupled regulation of multiple factors, including intercellular interactions, cellular activity, and mechanical constraints. A comprehensive understanding of the spatiotemporal dynamics of these surfaces and interfaces is essential for elucidating the structure–function relationship in biological tissues and the underlying mechanisms of disease progression. In this dissertation, we investigate the morphodynamic evolution of collective cellular surfaces and interfaces through a combination of cellular experiments, theoretical modeling, and numerical simulations.First, we examine the morphodynamics of tissue interfaces generated by cell sorting in mixed cell systems. Dynamic analysis reveals deformation waves propagating along the interface, highlighting the role of cellular activity in shaping the interface and driving wave propagation. Dispersion relation analysis confirms that activity-induced interfacial instability and coherent flow are the origin of these deformation waves. We further analyze the interaction between topological defects and the interface, as well as the spatial distribution of these defects. An active nematic model is employed to elucidate the underlying mechanism of interfacial fluctuations.Second, we investigate the effects of collective cell phase transitions on the formation and evolution of tissue interfaces and associated phase dynamics. We identify a caging transition induced by pulsed laser stimulation, which enables dynamic transitions under atypical conditions. The reversibility and dynamic properties of the transition are characterized, and a dynamical–topological coupling relation is proposed. The resulting flow–solid coupled interface significantly modulates both cell migration and energy distribution. A theoretical model based on deformable polygons successfully reproduces the dynamic and topological evolution driven by phase transitions, demonstrating the potential of this strategy for spatially tunable and contact-free surface and interface control.Finally, we explore the morphodynamics of three-dimensional tissue surfaces. A 3D interface experiment model is developed using collagen gel scaffolds, enabling quantitative analysis of collective cell behavior and cluster surface evolution across various cell lines. We characterize the effects of collective migration modes and their transitions on cluster surface morphology. By introducing global topological descriptors, we reveal the mechanisms of lumen formation, fusion, and topological transitions within the clusters.Collectively, this work establishes an integrated multi-scale, multi-method framework for understanding the dynamical evolution of collective cellular surfaces and interfaces. The findings advance fundamental knowledge in cellular collective dynamics and interface morphophysics, and offer new strategies and experimental foundations for the functional control of tissue surfaces and interfaces and the design of biomimetic systems.
