Bcl-2 prolongs cell survival after Bax-induced release of cytochrome c

Thierry Rossé, Reynald Olivier, Laurent Monney, Monika Rager, Sébastien Conus, Isabelle Fellay, Burkhard Jansen and Christoph Borner ()
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Thierry Rossé: Institute of Biochemistry, University of Fribourg
Reynald Olivier: Institute of Biochemistry, University of Fribourg
Laurent Monney: Institute of Biochemistry, University of Fribourg
Monika Rager: Institute of Biochemistry, University of Fribourg
Sébastien Conus: Institute of Biochemistry, University of Fribourg
Isabelle Fellay: Institute of Biochemistry, University of Fribourg
Burkhard Jansen: Vienna General Hospital, University of Vienna
Christoph Borner: Institute of Biochemistry, University of Fribourg

Nature, 1998, vol. 391, issue 6666, 496-499

Abstract: Abstract Following exposure of cells to stimuli that trigger programmed cell death (apoptosis), cytochrome c is rapidly released from mitochondria into the cytoplasm where it activates proteolytic molecules known as caspases that specifically cleave the amino-acid sequence DEVD and are crucial for the execution of apoptosis1,2,3,4. The protein Bcl-2 interferes with this activation of caspases by preventing the release of cytochrome c2,3,4. Here we study these molecular interactions during apoptosis induced by the protein Bax, a pro-apoptotic homologue of Bcl-2 (refs 5, 6). We show that in cells transiently transfected with bax, Bax localizes to mitochondria and induces the release of cytochrome c, activation of caspase-3, membrane blebbing, nuclear fragmentation, and cell death. Caspase inibitors do not affect Bax-induced cytochrome c release but block caspase-3 activation and nuclear fragmentation. Unexpectedly, Bcl-2 also fails to prevent Bax-induced cytochrome c release, although it co-localizes with Bax to mitochondria. Cells overexpressing both Bcl-2 and Bax show no signs of caspase activation and survive with significant amounts of cytochrome c in the cytoplasm. These findings indicate that Bcl-2 can interfere with Bax killing downstream of and independently of cytochrome c release.

Date: 1998
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DOI: 10.1038/35160

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