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MBC in Press, published online ahead of print March 19, 2008
Mol. Biol. Cell 10.1091/mbc.E07-09-0875

A more recent version of this article appeared on June 1, 2008 Originally published as MBC in Press, 10.1091/mbc.E07-09-0875 on March 26, 2008
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Submitted on September 7, 2007
Revised on March 3, 2008
Accepted on March 10, 2008

Id1 Overexpression Induces Tetraploidization and Multiple Abnormal Mitotic Phenotypes by Modulating Aurora A

Cornelia Man,* Jack Rosa,{dagger} Annie Lai-Man Cheung,* Y. L. Kwong,{ddagger} Stephen J. Doxsey,{dagger} and George Sai Wah Tsao*

*Department of Anatomy, and {ddagger}Department of Medicine, The University of Hong Kong, Pokfulam, Hong Kong SAR, China; {dagger}Program of Molecular Medicine, University of Massachusetts Medical School, Worcester, MA, 01605

Monitoring Editor: Orna Cohen-Fix

The basic helix-loop-helix transcription factor, Id1, was shown to induce tetraploidy in telomerase-immortalized nasopharyngeal epithelial cells in this study. Using both transient and stable Id1-expressing cell models, multiple mitotic aberrations were detected; including centrosome amplification, binucleation, spindle defects and microtubule perturbation. Many of these abnormal phenotypes have previously been reported in cells overexpressing Aurora A. Further experiments showed that Id1 could stabilize Aurora A, while knocking down Aurora A expression in Id1-expressing cells could rescue some of the mitotic defects. The mechanisms by which Aurora A could be modulated by Id1 were explored. DNA amplification of the Aurora A locus was not involved. Id1 could only weakly activate the transcriptional activity of the Aurora A promoter. We found that Id1 overexpression could affect Aurora A degradation, leading to its stabilization. Aurora A is normally degraded from mitosis exit by the APC/CCdh1-mediated proteasomal proteolysis pathway. Our results revealed that Id1 and Cdh1 are binding partners. The association of Id1 and Cdh1 was found to be dependent on the canonical destruction box (D box) motif of Id1; the increased binding of which may compete with the interaction between cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells.

Address correspondence to: George Sai Wah Tsao (gswtsao{at}hkucc.hku.hk)






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