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Title: Nek5 promotes centrosome integrity in interphase and loss of centrosome cohesion in mitosis
Authors: Prosser, Suzanna L.
Sahota, Navdeep K.
Pelletier, L.
Morrison, C. G.
Fry, Andrew M.
First Published: 11-May-2015
Publisher: Rockefeller University Press
Citation: Journal of Cell Biology, 2015, 209 (3), pp. 339-348 (10)
Abstract: Nek5 is a poorly characterized member of the NIMA-related kinase family, other members of which play roles in cell cycle progression and primary cilia function. Here, we show that Nek5, similar to Nek2, localizes to the proximal ends of centrioles. Depletion of Nek5 or overexpression of kinase-inactive Nek5 caused unscheduled separation of centrosomes in interphase, a phenotype also observed upon overexpression of active Nek2. However, separated centrosomes that resulted from Nek5 depletion remained relatively close together, exhibited excess recruitment of the centrosome linker protein rootletin, and had reduced levels of Nek2. In addition, Nek5 depletion led to loss of PCM components, including γ-tubulin, pericentrin, and Cdk5Rap2, with centrosomes exhibiting reduced microtubule nucleation. Upon mitotic entry, Nek5-depleted cells inappropriately retained centrosome linker components and exhibited delayed centrosome separation and defective chromosome segregation. Hence, Nek5 is required for the loss of centrosome linker proteins and enhanced microtubule nucleation that lead to timely centrosome separation and bipolar spindle formation in mitosis.
DOI Link: 10.1083/jcb.201412099
ISSN: 0021-9525
eISSN: 1540-8140
Version: Publisher Version
Status: Peer-reviewed
Type: Journal Article
Rights: This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 3.0 Unported license, as described at
Description: Supplemental Material can be found at
Appears in Collections:Published Articles, Dept. of Biochemistry

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