Shell Transformation Model for Simulating Cell Surface Structure

Abstract

The morphology of biological cells changes significantly when the cells carries out biological processes. These morphological changes are controlled by the plasma membrane, the biochemical signaling, and the actin network. The roles of plasma membrane and biochemical signaling have been studied extensively in the literature, while the roles of the actin network during these biological processes are less understood. For example, actin filaments are known to be active in clathrin-mediated endocytosis, phagocytosis, and viral budding. However, how a thin actin network is capable of producing the drastic morphological changes in these processes is still an open question from the mechanics point of view.

In this thesis research, a model is developed for investigating the deformation mechanisms of the cell surface structures during the biological process that involves significant morphological changes. The model consists of two parts: The first one is the mechanics of the cell surface structure, and this is taken into account by a thin shell theory that allows large deformation and finite elasticity in the system. The second part, on other hand, describes the changes in the cell surface structures when the cell carries out the biological processes. The changes are represented by transformation strains, forces, and dipoles in the shell. The model is termed the shell transformation model in this thesis.

The shell transformation model is applied to examine the pit formation and the invagination process during clathrin-mediated endocytosis, the viral budding, and the formation of pseudopodium during the phagocytosis. Of particular interest are the mechanisms that lead to the unique morphology observed in the experiments of the biological processes.