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Aurora-A overexpression reveals tetraploidization as a major route to centrosome amplification in p53(-/-) cells

MPG-Autoren
http://pubman.mpdl.mpg.de/cone/persons/resource/persons78390

Meraldi,  P.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78129

Honda,  R.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

http://pubman.mpdl.mpg.de/cone/persons/resource/persons78459

Nigg,  E. A.
Former Research Groups, Max Planck Institute of Biochemistry, Max Planck Society;

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Zitation

Meraldi, P., Honda, R., & Nigg, E. A. (2002). Aurora-A overexpression reveals tetraploidization as a major route to centrosome amplification in p53(-/-) cells. EMBO Journal, 21(4), 483-492.


Zitierlink: http://hdl.handle.net/11858/00-001M-0000-0010-6FB0-B
Zusammenfassung
Aberrations in centrosome numbers have long been implicated in aneuploidy and tumorigenesis, but their origins are unknown. Here we have examined how overexpression of Aurora-A kinase causes centrosome amplification in cultured cells. We show that excess Aurora-A does not deregulate centrosome duplication but gives rise to extra centrosomes through defects in cell division and consequent tetraploidization. Overexpression of other mitotic kinases (Polo-like kinase 1 and Aurora-B) also causes multinucleation and concomitant increases in centrosome numbers. Absence of a p53 checkpoint exacerbates this phenotype, providing a plausible explanation for the centrosome amplification typical of p53(-/-) cells. We propose that errors during cell division, combined with the inability to detect the resulting hyperploidy, constitute a major cause for numerical centrosome aberrations in tumors.