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An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis

Satdip Kaur, Andrew B. Fielding, Gisela Gassner, Nicholas J. Carter, View ORCID ProfileStephen J. Royle
doi: https://doi.org/10.1101/001701
Satdip Kaur
1Centre for Mechanochemical Cell Biology, Division of Biomedical Cell Biology, Warwick Medical School, University of Warwick, Coventry, CV4 7AL
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Andrew B. Fielding
2Department of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, L69 3BX
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Gisela Gassner
2Department of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, L69 3BX
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Nicholas J. Carter
1Centre for Mechanochemical Cell Biology, Division of Biomedical Cell Biology, Warwick Medical School, University of Warwick, Coventry, CV4 7AL
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Stephen J. Royle
1Centre for Mechanochemical Cell Biology, Division of Biomedical Cell Biology, Warwick Medical School, University of Warwick, Coventry, CV4 7AL
2Department of Cellular & Molecular Physiology, Institute of Translational Medicine, University of Liverpool, L69 3BX
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Abstract

Clathrin-mediated endocytosis (CME) is the major internalisation route for many different receptor types in mammalian cells. CME is shut down during early mitosis, but the mechanism of this inhibition is unclear. Here we show that the mitotic shutdown is due to an unmet requirement for actin in CME. In mitotic cells, membrane tension is increased and this invokes a requirement for the actin cytoskeleton to assist the CME machinery to overcome the increased load. However, the actin cytoskeleton is engaged in the formation of a rigid cortex in mitotic cells and is therefore unavailable for deployment. We demonstrate that CME can be “restarted” in mitotic cells despite high membrane tension, by allowing actin to engage in endocytosis. Mitotic phosphorylation of endocytic proteins is maintained in mitotic cells with restored CME, indicating that direct phosphorylation of the CME machinery does not account for shutdown.

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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 Unported 3.0 license.
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Posted January 09, 2014.
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An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis
Satdip Kaur, Andrew B. Fielding, Gisela Gassner, Nicholas J. Carter, Stephen J. Royle
bioRxiv 001701; doi: https://doi.org/10.1101/001701
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An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis
Satdip Kaur, Andrew B. Fielding, Gisela Gassner, Nicholas J. Carter, Stephen J. Royle
bioRxiv 001701; doi: https://doi.org/10.1101/001701

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