Calcium-mediated actin reset (CaAR) mediates acute cell adaptations

Wales P., Schuberth C., Aufschnaiter R., Fels J., García-Aguilar I., Janning A., Dlugos C., Schäfer-Herte M., Klingner C., Wälte M., Kuhlmann J., Menis E., Kang L., Maier K., Hou W., Russo A., Higgs H., Pavenstädt H., Vogl T., Roth J., Qualmann B., Kessels M., Martin D., Mulder B., Wedlich-Söldner R.

Abstract

Actin has well established functions in cellular morphogenesis. However, it is not well understood how the various actin assemblies in a cell are kept in a dynamic equilibrium, in particular when cells have to respond to acute signals. Here, we characterize a rapid and transient actin reset in response to increased intracellular calcium levels. Within seconds of calcium influx, the formin INF2 stimulates filament polymerization at the endoplasmic reticulum (ER), while cortical actin is disassembled. The reaction is then reversed within a few minutes. This Calcium-mediated actin reset (CaAR) occurs in a wide range of mammalian cell types and in response to many physiological cues. CaAR leads to transient immobilization of organelles, drives reorganization of actin during cell cortex repair, cell spreading and wound healing, and induces long-lasting changes in gene expression. Our findings suggest that CaAR acts as fundamental facilitator of cellular adaptations in response to acute signals and stress.

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