Profilin and formin constitute a pacemaker system for robust actin filament growth

Author:

Funk Johanna1ORCID,Merino Felipe2ORCID,Venkova Larisa3ORCID,Heydenreich Lina4,Kierfeld Jan4ORCID,Vargas Pablo3,Raunser Stefan2ORCID,Piel Matthieu3,Bieling Peter1ORCID

Affiliation:

1. Department of Systemic Cell Biology, Max Planck Institute of Molecular Physiology, Dortmund, Germany

2. Department of Structural Biochemistry, Max Planck Institute of Molecular Physiology, Dortmund, Germany

3. Institut Curie UMR144 CNRS, Paris, France

4. Physics Department, TU Dortmund University, Dortmund, Germany

Abstract

The actin cytoskeleton drives many essential biological processes, from cell morphogenesis to motility. Assembly of functional actin networks requires control over the speed at which actin filaments grow. How this can be achieved at the high and variable levels of soluble actin subunits found in cells is unclear. Here we reconstitute assembly of mammalian, non-muscle actin filaments from physiological concentrations of profilin-actin. We discover that under these conditions, filament growth is limited by profilin dissociating from the filament end and the speed of elongation becomes insensitive to the concentration of soluble subunits. Profilin release can be directly promoted by formin actin polymerases even at saturating profilin-actin concentrations. We demonstrate that mammalian cells indeed operate at the limit to actin filament growth imposed by profilin and formins. Our results reveal how synergy between profilin and formins generates robust filament growth rates that are resilient to changes in the soluble subunit concentration.

Funder

Human Frontier Science Program

Max Planck Society

Bundesministerium für Bildung und Forschung

Publisher

eLife Sciences Publications, Ltd

Subject

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

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