Modeling and Computation Seminar

Nearly 20 years ago, Neil Mendelson observed whirls and jets in dense colonies of Bacillus subtilis on top of agar.  This organized collective motion has since been shown to arise whenever swimming bacteria are at sufficient density.  Under appropriate conditions, hydrodynamic effects drive the alignment of nearby bacteria, but the dipole-distributed forces from the bacteria on the fluid destabilize the system and cause the formation of transient vortices and jets. When your skin gets cut, one of the first processes is re-epithelialization.  The top living layer of your skin, the epithelium, must heal itself, which is accomplished by the crawling of the epithelial cells over the wounded region.  Experiments have shown that this process involves elaborate coordinated cell motions that include whirling vortices. Are the similarities in these two disparate systems coincidence?  Or is there fundamental similarities in the physics that drives these two systems? Here I will discuss our attempts to construct mathematical models for these two systems that are grounded in the basic behaviour of the single cells that generate the motions.  An intriguing connection is that both swimming bacteria and crawling epithelial cells exert dipole-distributed forces on their surroundings.  In order to test these models, we have performed a number of experiments that produce unexpected results.  For example, it has been shown that confined suspensions of B. subtilis form a single, stable, counter-rotating vortex. However, we find that confined E. coli instead forms micro-spin cycles, a persistent periodically reversing vortex. What defines the marked difference between the collective dynamics of these two flagellated swimmers? And, in epithelial cells, perturbations that slow isolated cells are found to dramatically increase collective migration. I will show that our models naturally predict these behaviours and can quantitatively match our experimental data.  Then, because many cancers arise from epithelial tissues, I will conclude by arguing for a biophysical examination of the transition to metastasis in cancer and discuss how our epithelial cell model may provide insights that are currently obscured by traditional genomic and proteomic methodologies.