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

Kaur, Satdip and Fielding, Andrew B. and Gassner, Gisela and Carter, Nicholas J. and Royle, Stephen J. (2014) An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis. eLife, 3. ISSN 2050-084X

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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. In this study, 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. DOI: http://dx.doi.org/10.7554/eLife.00829.001.

Item Type:
Journal Article
Journal or Publication Title:
eLife
Uncontrolled Keywords:
/dk/atira/pure/subjectarea/asjc/2800
Subjects:
?? ACTIN CYTOSKELETONCELL CYCLECELL MEMBRANECLATHRINENDOCYTOSISHELA CELLSHUMANSMITOSISJOURNAL ARTICLERESEARCH SUPPORT, NON-U.S. GOV'TBIOCHEMISTRY, GENETICS AND MOLECULAR BIOLOGY(ALL)MEDICINE(ALL)IMMUNOLOGY AND MICROBIOLOGY(ALL)NEUROSCIENCE(ALL) ??
ID Code:
124293
Deposited By:
Deposited On:
28 Mar 2018 12:38
Refereed?:
Yes
Published?:
Published
Last Modified:
21 Sep 2023 02:23