Publication Date:
2022-05-25
Description:
© The Author(s), 2015. This article is distributed under the terms of the Creative Commons Attribution License. The definitive version was published in Molecular Biology of the Cell 26 (2015): 3424-3438, doi:10.1091/mbc.E15-02-0113.
Description:
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.
Description:
This work
was supported by a Wellcome Trust RCDF award (090064/Z/09/Z)
to E.R.G., a Wellcome Trust Strategic award to the Centre for Gene
Regulation and Expression (097945/B/11/Z), and a grant from the
German Research Foundation to A.H. (HU895/5-1). S.C. was supported
by a Biotechnology and Biological Sciences Research
Council studentship.
Repository Name:
Woods Hole Open Access Server
Type:
Article
Format:
application/pdf
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