Socialism vs. Rugged Individualism: Strengths and weaknesses in collective migration
Charles Wolgemuth; Associate Professor, University of Arizona
November 10 in the Fralin Auditorium, Fralin Hall 102
Hosted by Dr. J. Chen
Charles Wolgemuth is a professor of Physics and Molecular and Cellular Biology, at the University of Arizona. His current research focuses on understanding the biochemical and biophysical mechanisms that underlie eukaryotic cell crawling, the collective migration of cells during wound healing and cancer metastasis, and the pathogen-host interactions that occur during Lyme disease. His group utilizes a mix of computational modeling and experiments that typically involve live cell imaging to measure how biochemical, genetic, or environmental alterations alter the motility and/or growth of cells. Dr. Wolgemuth received his Ph.D. from the University of Arizona in 2000. After doing a postdoctoral fellowship at the University of California, Berkeley, working with George Oster, he took a faculty position in the Department of Cell Biology and the Richard D. Berlin Center for Cell Analysis and Modeling at the University of Connecticut Health Center before moving back to University of Arizona.
Multicellular organisms require groups of cells to function together as a unit. A common scenario involves the collective movement of cells. For example, when your skin gets cut, one of the first processes is re-epithelialization where epidermal cells crawl over the wounded region. Likewise, in cancer, tumor cells often move as a group to detach from the primary tumor and invade distal regions of the body. In this presentation, I will describe the work that we have been doing to develop a multiscale model for collective cell migration. This model is based in the fundamental biophysics of a single cell. We show that a combination of directed cell motility, dipole-distributed forces, and adhesion to neighboring cells and the environment is sufficient to explain in vitro wound healing dynamics and gives insight into the biophysical changes that occur when cancer cells become metastatic. This model provides testable predictions; for example, the rate of wound healing should be proportional to the contractile stress that the cells exert on their surroundings. We use experiments to probe the predictions of the model and find some surprising results that weren’t expected but should have been.