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Targeting of the pro‐apoptotic VDAC‐like porin (PorB) of Neisseria gonorrhoeae to mitochondria of infected cells
Author(s) -
Müller Anne,
Günther Dirk,
Brinkmann Volker,
Hurwitz Robert,
Meyer Thomas F.,
Rudel Thomas
Publication year - 2000
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1093/emboj/19.20.5332
Subject(s) - neisseria gonorrhoeae , porin , biology , voltage dependent anion channel , mitochondrion , bacterial outer membrane , microbiology and biotechnology , apoptosis , virology , oomycete , escherichia coli , genetics , gene , pathogen
Infection of cell cultures with Neisseria gonorrhoeae results in apoptosis that is mediated by the PorB porin. During the infection process porin translocates from the outer bacterial membrane into host cell membranes where its channel activity is regulated by nucleotide binding and voltage‐dependent gating, features that are shared by the mitochondrial voltage‐dependent anion channel (VDAC). Here we show that porin is selectively and efficiently transported to mitochondria of infected cells. Prevention of porin translocation also blocked the induction of apoptosis. Mitochondria of cells treated with porin both in vitro and in vivo were depleted of cytochrome c and underwent permeability transition. Overexpression of Bcl‐2 blocked porin‐induced apoptosis. The release of cytochrome c occurred independently of active caspases but was completely prevented by Bcl‐2. Our data suggest that the Neisseria porin can, like its eukaryotic homologue, function at the mitochondrial checkpoint to mediate apoptosis.