2. Academic Validation
  3. The nucleoporin ALADIN regulates Aurora A localization to ensure robust mitotic spindle formation

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

  • Mol Biol Cell. 2015 Oct 1;26(19):3424-38. doi: 10.1091/mbc.E15-02-0113.
Sara Carvalhal 1,  Susana Abreu Ribeiro 2,  Miguel Arocena 1,  Taciana Kasciukovic 1,  Achim Temme 3,  Katrin Koehler 4,  Angela Huebner 4,  Eric R Griffis 5
Affiliations

Affiliations

  • 1 Centre for Gene Regulation and Expression, University of Dundee, College of Life Sciences, Dundee DD1 5EH, United Kingdom.
  • 2 Physiology Course, Marine Biological Laboratory, Woods Hole, MA 02543 Wellcome Trust Centre for Cell Biology, Institute of Cell and Molecular Biology, University of Edinburgh, Edinburgh EH9 3JR, United Kingdom.
  • 3 Department of Neurosurgery, University Hospital Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany.
  • 4 Department of Paediatrics, University Hospital Carl Gustav Carus, Technische Universität Dresden, D-01307 Dresden, Germany.
  • 5 Centre for Gene Regulation and Expression, University of Dundee, College of Life Sciences, Dundee DD1 5EH, United Kingdom Physiology Course, Marine Biological Laboratory, Woods Hole, MA 02543 [email protected].
PMID: 26246606 DOI: 10.1091/mbc.E15-02-0113
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 ALADIN is a novel spatial regulator of Aurora A. Without ALADIN, Aurora A spreads 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. Of interest, mutations in ALADIN cause triple A syndrome. We find that 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 part of the etiology of this syndrome.

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