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Papers In Press, published online ahead of print March 20, 2001
J. Biol. Chem, 10.1074/jbc.M101590200
Submitted on February 20, 2001
Revised on March 15, 2001
Accepted on March 20, 2001

Bcl-xL promotes the open configuration of VDAC and metabolite passage through the outer mitochondrial membrane

Matthew G. Vander Heiden, Xiao Xian Li, Eyal Gottlieb, R. Blake Hill, Craig B. Thompson, and Marco Colombini

Cancer Biology, University of Pennsylvania, Philadelphia, PA 19104

Corresponding Author: drt{at}mail.med.upenn.edu

The diffusion of metabolites across the outer mitochondrial membrane is essential for coupled cellular respiration. The outer membrane of mitochondria isolated from growth factor-deprived cells is impaired in its ability to exchange metabolic anions. When added to mitochondria, recombinant Bcl-xL restores metabolite exchange across the outer membrane, without inducing the loss of cytochrome c from the intermembrane space. Restoration of outer membrane permeability to anionic metabolites does not occur directly through Bcl-xL ion channels. Instead, recombinant Bcl-xL maintains the outer mitochondrial membrane channel, VDAC, in an open configuration. Consistent with these findings, when ADP-induced oxidative phosphorylation is limited by exogenous bNADH, recombinant Bcl-xL can sustain outer mitochondrial membrane permeability to ADP. b-NADH limits respiration by promoting the closed configuration of VDAC. Together these results demonstrate that following an apoptotic signal, Bcl-xL can maintain metabolite exchange across the outer mitochondrial membrane by inhibiting VDAC closure.


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