Abstract
The viscosity of the plasma membrane in living cells is a crucial biophysical parameter that regulates cellular functions. We categorize the plasma membrane viscosity into short-range and long-range viscosities based on the spatial scale of the cellular processes they influence. Short-range viscosity originates from the Brownian motion of membrane molecules (i.e., the nanometer-scale motion of molecules) and regulates signal transduction and membrane transport. It is reported that the short-range viscosity in living cells is almost the same or at most 10 times greater than that of 1,2-dioleoyl-sn-glycero-3-phosphocholine (DOPC) membranes. In contrast, long-range viscosity is critical for cellular-scale (i.e., micrometer scale) membrane flow, which plays important roles during cell migration and cell division. The long-range membrane viscosity in living cells is expected to include the effect of complicated cellular structures, such as the actomyosin-based cellular cortex, and thus differs significantly from the short-range viscosity. In this study, we measure the long-range viscosity in living cells, for the first time to our knowledge, by applying an external force to the plasma membrane of the C. elegans embryo. In intact cells, membrane flow was not induced by applied external forces. When the polymerization of the actin cytoskeleton was inhibited, the external force induced a pair of vortex flows across the plasma membrane. The vortex flow pattern was compared to a hydrodynamic model, and long-range viscosity in living cells was determined. Our measurement revealed that the long-range viscosity was four orders of magnitude greater than both DOPC membranes and the short-range viscosity in living cells. The factors contributing to the four orders of magnitude higher viscosity of plasma membranes compared with DOPC GUVs were discussed in relation to actin organization after polymerization inhibition.