Multicellular behavior in bacterial biofilms is intimately tied to the production of an extracellular polysaccharide (EPS) matrix that encases the cells and provides physical integrity to the colony as a whole. As a colony grows from a few cells into a biofilm, a sudden increase in EPS production generates osmotic stresses that cause the biofilm to expand. Moreover, EPS production is triggered by a nutrient depletion gradient that develops in the biofilm due to diffusive mass transport limitations. These polymer physics based biofilm behaviors suggest that EPS production may have evolved in biofilms to beat the diffusion limit of nutrient transport into the colony, though no direct observation of nutrient transport has been observed previously. In this talk I will discuss measurements of nutrient transport into b. subtilis biofilms and show that when EPS production is up-regulated, the polymer sucks fluid into the colony with a characteristic time dependence like that of pressure driven flow.
In contrast to bacteria in biofilms, eukaryotic cell behavior in tissues is intimately tied to forces generated by molecular motor-driven contractions. Contraction generated tensions are balanced by deformations in the cell's microenvironment, by internal cytoskeletal structures, and by the incompressible cytosolic fluid contained within the cell membrane. However, contraction generated pressures cannot be supported by the cytosol if the cell membrane is adequately permeable. Small, non-selective pores called gap junctions connect cells in a layer, allowing small molecules to pass between cells. In the second half of this talk I will discuss measurements of contraction driven fluid movement across gap junctions connecting neighboring cells. We observe contracting cells pushing fluid into their neighbors. To study the mechanics of intercellular fluid flow, we apply biologically relevant pressures to large regions of cells in a monolayer with a micro-indentation system. We directly measure indentation force and volume as a function of time to determine fluid flow rates and associated stresses between cells. We find that gap-junction permeability does not limit fluid transport between cells, and that fluid flow is controlled by a balance of cytoskeletal tension throughout the cell monolayer.