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Type-I myosins promote actin polymerization to drive membrane bending in endocytosis

View ORCID ProfileHetty E. Manenschijn, View ORCID ProfileAndrea Picco, View ORCID ProfileMarkus Mund, View ORCID ProfileJonas Ries, View ORCID ProfileMarko Kaksonen
doi: https://doi.org/10.1101/490011
Hetty E. Manenschijn
1Department of Biochemistry, University of Geneva, Geneva, Switzerland
2Cell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany
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Andrea Picco
1Department of Biochemistry, University of Geneva, Geneva, Switzerland
3NCCR Chemical Biology, University of Geneva, Geneva, Switzerland
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Markus Mund
1Department of Biochemistry, University of Geneva, Geneva, Switzerland
2Cell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany
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Jonas Ries
2Cell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany
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Marko Kaksonen
1Department of Biochemistry, University of Geneva, Geneva, Switzerland
3NCCR Chemical Biology, University of Geneva, Geneva, Switzerland
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Abstract

Clathrin-mediated endocytosis in budding yeast requires the formation of a dynamic actin network that produces the force to invaginate the plasma membrane against the intracellular turgor pressure. The type-I myosins Myo3 and Myo5 are important for endocytic membrane reshaping, but mechanistic details of their function remain scarce. Here, we studied the function of Myo3 and Myo5 during endocytosis using quantitative live-cell imaging and genetic perturbations. We show that the type-I myosins promote, in a dose-dependent way, the growth and expansion of the actin network, which controls the speed of membrane and coat internalization. We found that this myosin-activity is independent of the actin nucleation promoting activity of myosins, and cannot be compensated for by increasing actin nucleation. Our results suggest a new mechanism for type-I myosins to produce force by promoting actin filament polymerization.

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The copyright holder for this preprint is the author/funder, who has granted bioRxiv a license to display the preprint in perpetuity. It is made available under a CC-BY-ND 4.0 International license.
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Posted December 09, 2018.
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Type-I myosins promote actin polymerization to drive membrane bending in endocytosis
Hetty E. Manenschijn, Andrea Picco, Markus Mund, Jonas Ries, Marko Kaksonen
bioRxiv 490011; doi: https://doi.org/10.1101/490011
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Type-I myosins promote actin polymerization to drive membrane bending in endocytosis
Hetty E. Manenschijn, Andrea Picco, Markus Mund, Jonas Ries, Marko Kaksonen
bioRxiv 490011; doi: https://doi.org/10.1101/490011

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