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

Author:

Wales Pauline12,Schuberth Christian E12,Aufschnaiter Roland12,Fels Johannes12,García-Aguilar Ireth3ORCID,Janning Annette12,Dlugos Christopher P124,Schäfer-Herte Marco12,Klingner Christoph125,Wälte Mike12,Kuhlmann Julian12,Menis Ekaterina12,Hockaday Kang Laura12,Maier Kerstin C6,Hou Wenya7,Russo Antonella8,Higgs Henry N9,Pavenstädt Hermann4,Vogl Thomas8,Roth Johannes8,Qualmann Britta7,Kessels Michael M7,Martin Dietmar E6,Mulder Bela3,Wedlich-Söldner Roland12ORCID

Affiliation:

1. Institute of Cell Dynamics and Imaging, University of Muenster, Muenster, Germany

2. Cells-In-Motion Cluster of Excellence (EXC1003 – CiM), University of Münster, Muenster, Germany

3. Theory of Biological Matter, FOM Institute AMOLF, Amsterdam, Netherlands

4. Medical Clinic D, University Clinic of Muenster, Muenster, Germany

5. AG Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Munich, Germany

6. Department of Biochemistry, University of Munich, Munich, Germany

7. Institute of Biochemistry I, Friedrich Schiller University Jena, Jena, Germany

8. Institute of Immunology, University of Münster, Münster, Germany

9. Department of Biochemistry, Dartmouth Medical School, Hanover, United States

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.

Funder

Deutsche Forschungsgemeinschaft

Max-Planck-Gesellschaft

University of Münster

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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