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Published online
doi:10.1083/jcb.200702134
The Journal of Cell Biology, Vol. 178, No. 2, 283-296
The Rockefeller University Press, 0021-9525 $30.00
© Niikura et al.
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Article

BUB1 mediation of caspase-independent mitotic death determines cell fate



Yohei Niikura1, Amruta Dixit2, Ray Scott2, Guy Perkins2, and Katsumi Kitagawa1

1 Department of Molecular Pharmacology, St. Jude Children's Research Hospital, Memphis, TN 38105
2 National Center for Microscopy and Imaging Research, Center for Research on Biological Structure, School of Medicine, University of California, San Diego, La Jolla, CA 92093

Correspondence to Katsumi Kitagawa: katsumi.kitagawa{at}stjude.org

The spindle checkpoint that monitors kinetochore–microtubule attachment has been implicated in tumorigenesis; however, the relation between the spindle checkpoint and cell death remains obscure. In BUB1-deficient (but not MAD2-deficient) cells, conditions that activate the spindle checkpoint (i.e., cold shock or treatment with nocodazole, paclitaxel, or 17-AAG) induced DNA fragmentation during early mitosis. This mitotic cell death was independent of caspase activation; therefore, we named it caspase-independent mitotic death (CIMD). CIMD depends on p73, a homologue of p53, but not on p53. CIMD also depends on apoptosis-inducing factor and endonuclease G, which are effectors of caspase-independent cell death. Treatment with nocodazole, paclitaxel, or 17-AAG induced CIMD in cell lines derived from colon tumors with chromosome instability, but not in cells from colon tumors with microsatellite instability. This result was due to low BUB1 expression in the former cell lines. When BUB1 is completely depleted, aneuploidy rather than CIMD occurs. These results suggest that cells prone to substantial chromosome missegregation might be eliminated via CIMD.

Abbreviations used in this paper: AIF, apoptosis-inducing factor; CIMD, caspase-independent mitotic death; CIN, chromosome instability; EndoG, endonuclease G; MIN, microsatellite instability; siRNA, small interfering RNA; TEM, transmission electron microscopy.


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