The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation

Sara Carvalhal; Susana Abreu Ribeiro; Miguel Arocena; Taciana Kasciukovic; Achim Temme; Katrin Koehler; Angela Huebner; Eric R. Griffis

doi:10.1091/mbc.E15-02-0113

The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation

Sara Carvalhal, Susana Abreu Ribeiro, Miguel Arocena, Taciana Kasciukovic, Achim Temme, Katrin Koehler, Angela Huebner, Eric R. Griffis (Lead / Corresponding author)

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Abstract

The formation of the mitotic spindle is a complex process that requires massive cellular reorganization. Regulation by mitotic kinases controls this entire process. One of these mitotic controllers is Aurora A kinase, which is itself highly regulated. In this study we show that the nuclear pore protein 2

ALADIN is a novel spatial regulator of Aurora A. Without ALADIN, we observe Aurora A spreading from centrosomes onto spindle microtubules, which affects the distribution of a subset of microtubule regulators and slows spindle assembly and chromosome alignment. ALADIN interacts with inactive Aurora A and is recruited to the spindle pole after Aurora A inhibition. Curiously, mutations in ALADIN cause triple A syndrome. We find some of the mitotic phenotypes that we observe after ALADIN depletion also occur in cells from triple A syndrome patients, which raises the possibility that mitotic errors may underlie the etiology of this syndrome.

Original language	English
Pages (from-to)	3424-3438
Number of pages	15
Journal	Molecular Biology of the Cell
Volume	26
Issue number	19
Early online date	5 Aug 2015
DOIs	https://doi.org/10.1091/mbc.E15-02-0113
Publication status	Published - 1 Oct 2015

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10.1091/mbc.E15-02-0113Licence: CC BY-NC-SA

Final Published Version
© 2015 Carvalhal et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).
Final published version, 7.68 MBLicence: CC BY-NC-SA

Strategic Award: Wellcome Trust Technology Platform
Blow, J. (Investigator), Lamond, A. (Investigator) & Owen-Hughes, T. (Investigator)
1/01/13 → 30/09/18
Project: Research

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title = "The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation",

abstract = "The formation of the mitotic spindle is a complex process that requires massive cellular reorganization. Regulation by mitotic kinases controls this entire process. One of these mitotic controllers is Aurora A kinase, which is itself highly regulated. In this study we show that the nuclear pore protein 2 ALADIN is a novel spatial regulator of Aurora A. Without ALADIN, we observe Aurora A spreading from centrosomes onto spindle microtubules, which affects the distribution of a subset of microtubule regulators and slows spindle assembly and chromosome alignment. ALADIN interacts with inactive Aurora A and is recruited to the spindle pole after Aurora A inhibition. Curiously, mutations in ALADIN cause triple A syndrome. We find some of the mitotic phenotypes that we observe after ALADIN depletion also occur in cells from triple A syndrome patients, which raises the possibility that mitotic errors may underlie the etiology of this syndrome.",

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AU - Carvalhal, Sara

AU - Abreu Ribeiro, Susana

AU - Arocena, Miguel

AU - Kasciukovic, Taciana

AU - Temme, Achim

AU - Koehler, Katrin

AU - Huebner, Angela

AU - Griffis, Eric R.

PY - 2015/10/1

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N2 - The formation of the mitotic spindle is a complex process that requires massive cellular reorganization. Regulation by mitotic kinases controls this entire process. One of these mitotic controllers is Aurora A kinase, which is itself highly regulated. In this study we show that the nuclear pore protein 2 ALADIN is a novel spatial regulator of Aurora A. Without ALADIN, we observe Aurora A spreading from centrosomes onto spindle microtubules, which affects the distribution of a subset of microtubule regulators and slows spindle assembly and chromosome alignment. ALADIN interacts with inactive Aurora A and is recruited to the spindle pole after Aurora A inhibition. Curiously, mutations in ALADIN cause triple A syndrome. We find some of the mitotic phenotypes that we observe after ALADIN depletion also occur in cells from triple A syndrome patients, which raises the possibility that mitotic errors may underlie the etiology of this syndrome.

AB - The formation of the mitotic spindle is a complex process that requires massive cellular reorganization. Regulation by mitotic kinases controls this entire process. One of these mitotic controllers is Aurora A kinase, which is itself highly regulated. In this study we show that the nuclear pore protein 2 ALADIN is a novel spatial regulator of Aurora A. Without ALADIN, we observe Aurora A spreading from centrosomes onto spindle microtubules, which affects the distribution of a subset of microtubule regulators and slows spindle assembly and chromosome alignment. ALADIN interacts with inactive Aurora A and is recruited to the spindle pole after Aurora A inhibition. Curiously, mutations in ALADIN cause triple A syndrome. We find some of the mitotic phenotypes that we observe after ALADIN depletion also occur in cells from triple A syndrome patients, which raises the possibility that mitotic errors may underlie the etiology of this syndrome.

U2 - 10.1091/mbc.E15-02-0113

DO - 10.1091/mbc.E15-02-0113

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JO - Molecular Biology of the Cell

JF - Molecular Biology of the Cell

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ER -

The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation

Abstract

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Strategic Award: Wellcome Trust Technology Platform

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