Control of apoptosis and mitotic spindle checkpoint by survivin

Fengzhi Li, Grazia Ambrosini, Emily Y. Chu, Janet Plescia, Simona Tognin, Pier Carlo Marchisio and Dario C. Altieri ()
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Fengzhi Li: Boyer Center for Molecular Medicine, Yale University School of Medicine
Grazia Ambrosini: Boyer Center for Molecular Medicine, Yale University School of Medicine
Emily Y. Chu: Boyer Center for Molecular Medicine, Yale University School of Medicine
Janet Plescia: Boyer Center for Molecular Medicine, Yale University School of Medicine
Simona Tognin: DIBIT S. Raffaele Scientific Institute
Pier Carlo Marchisio: DIBIT S. Raffaele Scientific Institute
Dario C. Altieri: Boyer Center for Molecular Medicine, Yale University School of Medicine

Nature, 1998, vol. 396, issue 6711, 580-584

Abstract: Abstract Progression of the cell cycle and control of apoptosis (programmed cell death) are thought to be intimately linked processes1, acting to preserve homeostasis and developmental morphogenesis2. Although proteins that regulate apoptosis have been implicated in restraining cell-cycle entry3 and controlling ploidy (chromosome number)4, the effector molecules at the interface between cell proliferation and cell survival have remained elusive. Here we show that a new inhibitor of apoptosis (IAP) protein5,6, survivin7, is expressed in the G2/M phase of the cell cycle in a cycle-regulated manner. At the beginning of mitosis, survivin associates with microtubules of the mitotic spindle in a specific and saturable reaction that is regulated by microtubule dynamics8. Disruption of survivin–microtubule interactions results in loss of survivin's anti-apoptosis function and increased caspase-3 activity, a mechanism involved in cell death, during mitosis. These results indicate that survivin may counteract a default induction of apoptosis in G2/M phase. The overexpression of survivin in cancer7 may overcome this apoptotic checkpoint and favour aberrant progression of transformed cells through mitosis.

Date: 1998
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DOI: 10.1038/25141

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