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Vol. 15, Issue 7, 3061-3072, July 2004
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* Department of Pathology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261;
|| Department of Neurology, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15261;
Department of Biochemistry, Chosun University School of Medicine, Gwangju, 501-759, Korea; and
Korea Basic Science Institute Gwangju Branch, Chonnam National University, Gwangju, 500-757, Korea
Submitted December 1, 2003;
Revised April 8, 2004;
Accepted April 9, 2004
Monitoring Editor: Randy Schekman
Release of cytochrome c from the mitochondrial intermembrane space is critical to apoptosis induced by a variety of death stimuli. Bid is a BH3-only prodeath Bcl-2 family protein that can potently activate this efflux. In the current study, we investigated the mitochondrial localization of Bid and its interactions with mitochondrial phospholipids, focusing on their relationships with Bid-induced cytochrome c release. We found that Bid binding to the mitochondria required only three of its eight helical structures (
4-6), but not the BH3 domain, and the binding could not be inhibited by the antideath molecule Bcl-xL. Membrane fractionations indicated that tBid bound to mitochondrial outer membranes at both contact and noncontact sites. Bid could interact with specific cardiolipin species on intact mitochondria as identified by mass spectrometry. Like the binding to the mitochondria, this interaction could not be blocked by the mutation in the BH3 domain or by Bcl-xL. However, a cardiolipin-specific dye, 10-N-nonyl acridine orange, could preferentially suppress Bid binding to the mitochondrial contact site and inhibit Bid-induced mitochondrial cristae reorganization and cytochrome c release. These findings thus suggest that interactions of Bid with mitochondrial cardiolipin at the contact site can contribute significantly to its functions.
These authors contributed equally to this study.
¶ Corresponding author. E-mail address: xmyin{at}pitt.edu.
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