Cell polarization as a possible mechanism of response termination.

Neutrophils stimulated with a low concentration of chemotactic peptide N-formyl-met-leu-phe respond with a brief pulse of actin polymerization and a persistent change in morphology from round to polarized. The recovery of the actin polymerization response is unlikely to be due to usual receptor desensitization mechanisms. We hypothesized that cell polarization and redistribution of signaling components effect the depolymerization phase of the actin response. In this report we show that the overall actin depolymerization is equivalent to the reduction in the volume occupied by F-actin while its concentration at the front of the polarized cell remains undiminished. To test whether the confinement of F-actin to a small volume can be caused by receptor redistribution, we observed receptors and F-actin in the same cell and found that their localization was different. To explain our findings, we propose a model based on the affinity of a signaling component, other than the receptor, for the areas of the cell rich in F-actin.