This lecture covers the biochemical basis of actin-based motility (focusing on the pathogen Listeria as a model system for this process), the biophysical mechanism of polymerization-based force generation, and an evolutionary perspective of cell shape in prokaryotes and eukaryotes. The first part covers our understanding of how cells use the actin cytoskeleton to crawl. The pathogenic bacteria Listeria (which causes food poisoning) uses the actin cytoskeleton to propel itself in the cytoplasm and also invade other cells. This system has been an important model for understanding the actin cytoskeleton at the leading edge of a motile cell and for understanding host-pathogen interactions.
The second part is devoted to understanding how the polymerization of actin can produce, which is a current area of research in our laboratory. Here, I cover theories for how polymerization might be used to produce forces, and our efforts to test these models using optical traps, atomic force microscopes, and nanofabricated devices.
In the third part, I discuss how the complex shapes of cells are created by the cytoskeleton, and I compare and contrast prokaryotes (which have actin-, tubulin-, and intermediate filament -like proteins) and eukaryotes in this regard. In particular, I speculate that cytoskeletal dynamics were necessary to evolve simple bacterial shapes and cell division, but that additional layers of complexity (namely regulated nucleation and molecular motors) allowed eukaryotes to evolve more complex shapes and organize their internal components.