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Published online May 21, 2007
doi:10.1083/jcb.200610148
The Journal of Cell Biology, Vol. 177, No. 4, 625-636
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Weber et al.
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Article

BimS-induced apoptosis requires mitochondrial localization but not interaction with anti-apoptotic Bcl-2 proteins



Arnim Weber1, Stefan A. Paschen1, Klaus Heger1, Florian Wilfling1, Tobias Frankenberg1, Heike Bauerschmitt2, Barbara M. Seiffert1, Susanne Kirschnek1, Hermann Wagner1, and Georg Häcker1

1 Institute for Medical Microbiology, Immunology, and Hygiene, Technische Universität München, D-81675 Munich, Germany
2 Adolf-Butenandt-Institut für Physiologische Chemie der LMU München, D-81377 Munich, Germany

Correspondence to Georg Häcker: hacker{at}lrz.tum.de

Release of apoptogenic proteins such as cytochrome c from mitochondria is regulated by pro- and anti-apoptotic Bcl-2 family proteins, with pro-apoptotic BH3-only proteins activating Bax and Bak. Current models assume that apoptosis induction occurs via the binding and inactivation of anti-apoptotic Bcl-2 proteins by BH3-only proteins or by direct binding to Bax. Here, we analyze apoptosis induction by the BH3-only protein BimS. Regulated expression of BimS in epithelial cells was followed by its rapid mitochondrial translocation and mitochondrial membrane insertion in the absence of detectable binding to anti-apoptotic Bcl-2 proteins. This caused mitochondrial recruitment and activation of Bax and apoptosis. Mutational analysis of BimS showed that mitochondrial targeting, but not binding to Bcl-2 or Mcl-1, was required for apoptosis induction. In yeast, BimS enhanced the killing activity of Bax in the absence of anti-apoptotic Bcl-2 proteins. Thus, cell death induction by a BH3-only protein can occur through a process that is independent of anti-apoptotic Bcl-2 proteins but requires mitochondrial targeting.

Abbreviations used in this paper: BH, Bcl-2 homology; IP, immunoprecipitation; tet, tetracycline.


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