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

Research output: Contribution to Journal/Magazine › Journal article › peer-review

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An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis. / Kaur, Satdip; Fielding, Andrew B.; Gassner, Gisela et al.
In: eLife, Vol. 3, e00829, 18.02.2014.

Research output: Contribution to Journal/Magazine › Journal article › peer-review

Harvard

Kaur, S, Fielding, AB, Gassner, G, Carter, NJ & Royle, SJ 2014, 'An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis', eLife, vol. 3, e00829. https://doi.org/10.7554/eLife.00829

APA

Kaur, S., Fielding, A. B., Gassner, G., Carter, N. J., & Royle, S. J. (2014). An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis. eLife, 3, Article e00829. https://doi.org/10.7554/eLife.00829

Vancouver

Kaur S, Fielding AB, Gassner G, Carter NJ, Royle SJ. An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis. eLife. 2014 Feb 18;3:e00829. doi: 10.7554/eLife.00829

Author

Kaur, Satdip ; Fielding, Andrew B. ; Gassner, Gisela et al. / An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis. In: eLife. 2014 ; Vol. 3.

Bibtex

@article{2e80ba6ecd854a4db9c90370db05134f,
title = "An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis",
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.",
keywords = "Actin Cytoskeleton, Cell Cycle, Cell Membrane, Clathrin, Endocytosis, HeLa Cells, Humans, Mitosis, Journal Article, Research Support, Non-U.S. Gov't",
author = "Satdip Kaur and Fielding, {Andrew B.} and Gisela Gassner and Carter, {Nicholas J.} and Royle, {Stephen J.}",
year = "2014",
month = feb,
day = "18",
doi = "10.7554/eLife.00829",
language = "English",
volume = "3",
journal = "eLife",
issn = "2050-084X",
publisher = "eLife Sciences Publications",

}

RIS

TY - JOUR

T1 - An unmet actin requirement explains the mitotic inhibition of clathrin-mediated endocytosis

AU - Kaur, Satdip

AU - Fielding, Andrew B.

AU - Gassner, Gisela

AU - Carter, Nicholas J.

AU - Royle, Stephen J.

PY - 2014/2/18

Y1 - 2014/2/18

N2 - 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.

AB - 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.

KW - Actin Cytoskeleton

KW - Cell Cycle

KW - Cell Membrane

KW - Clathrin

KW - Endocytosis

KW - HeLa Cells

KW - Humans

KW - Mitosis

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.7554/eLife.00829

DO - 10.7554/eLife.00829

M3 - Journal article

C2 - 24550251

VL - 3

JO - eLife

JF - eLife

SN - 2050-084X

M1 - e00829

ER -