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

By Satdip Kaur, Andrew B Fielding, Gisela Gassner, Nicholas J Carter, Stephen J Royle

Posted 09 Jan 2014
bioRxiv DOI: 10.1101/001701 (published DOI: 10.7554/eLife.00829)

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. Now published as eLife DOI: http://dx.doi.org/10.7554/eLife.00829

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