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through βTrCP-dependent degradation of hBora

By Eunice H. Y. Chan, Anna Santamaria, Herman H. W. Silljé, Erich A. Nigg, E. H. Y. Chan and H. H. W. Silljé


Abstract Polo-like kinase 1 (Plk1) and Aurora A play key roles in centrosome maturation, spindle assembly, and chromosome segregation during cell division. Here we show that the functions of these kinases during early mitosis are coordinated through Bora, a partner of Aurora A first identified in Drosophila. Depletion of human Bora (hBora) results in spindle defects, accompanied by increased spindle recruitment of Aurora A and its partner TPX2. Conversely, hBora overexpression induces mislocalization of Aurora A and monopolar spindle formation, reminiscent of the phenotype seen in Plk1-depleted cells. Indeed, Plk1 regulates hBora. Following Cdk1-dependent recruitment, Plk1 triggers hBora destruction by phosphorylating a recognition site for SCF " TrCP. Plk1 depletion or inhibition Communicated by: C. Lehner Electronic supplementary material The online version of this article (doi:10.1007/s00412-008-0165-5) contains supplementary material, which is available to authorized users

Year: 2013
DOI identifier: 10.1007/s00412-008-0165-5)
OAI identifier: oai:CiteSeerX.psu:
Provided by: CiteSeerX
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