Click here to close Hello! We notice that you are using Internet Explorer, which is not supported by Xenbase and may cause the site to display incorrectly. We suggest using a current version of Chrome, FireFox, or Safari.
XB-ART-53306
J Cell Biol August 3, 2015; 210 (3): 373-83.
Show Gene links Show Anatomy links

TPX2 phosphorylation maintains metaphase spindle length by regulating microtubule flux.

Fu J , Bian M , Xin G , Deng Z , Luo J , Guo X , Chen H , Wang Y , Jiang Q , Zhang C .


Abstract
A steady-state metaphase spindle maintains constant length, although the microtubules undergo intensive dynamics. Tubulin dimers are incorporated at plus ends of spindle microtubules while they are removed from the minus ends, resulting in poleward movement. Such microtubule flux is regulated by the microtubule rescue factors CLASPs at kinetochores and depolymerizing protein Kif2a at the poles, along with other regulators of microtubule dynamics. How microtubule polymerization and depolymerization are coordinated remains unclear. Here we show that TPX2, a microtubule-bundling protein and activator of Aurora A, plays an important role. TPX2 was phosphorylated by Aurora A during mitosis. Its phospho-null mutant caused short metaphase spindles coupled with low microtubule flux rate. Interestingly, phosphorylation of TPX2 regulated its interaction with CLASP1 but not Kif2a. The effect of its mutant in shortening the spindle could be rescued by codepletion of CLASP1 and Kif2a that abolished microtubule flux. Together we propose that Aurora A-dependent TPX2 phosphorylation controls mitotic spindle length through regulating microtubule flux.

PubMed ID: 26240182
PMC ID: PMC4523612
Article link: J Cell Biol


Species referenced: Xenopus
Genes referenced: aurka clasp1 kif2a tpx2


Article Images: [+] show captions
References [+] :
Bird, Building a spindle of the correct length in human cells requires the interaction between TPX2 and Aurora A. 2008, Pubmed