TY - JOUR A1 - Kozjak-Pavlovic, Vera A1 - Dian-Lothrop, Elke A. A1 - Meinecke, Michael A1 - Kepp, Oliver A1 - Ross, Katharina A1 - Rajalingam, Krishnaraj A1 - Harsman, Anke A1 - Hauf, Eva A1 - Brinkmann, Volker A1 - Günther, Dirk A1 - Herrmann, Ines A1 - Hurwitz, Robert A1 - Rassow, Joachim A1 - Wagner, Richard A1 - Rudel, Thomas T1 - Bacterial porin disrupts mitochondrial membrane potential and sensitizes host cells to apoptosis T2 - PLoS pathogens N2 - The bacterial PorB porin, an ATP-binding beta-barrel protein of pathogenic Neisseria gonorrhoeae, triggers host cell apoptosis by an unknown mechanism. PorB is targeted to and imported by host cell mitochondria, causing the breakdown of the mitochondrial membrane potential (delta psi m). Here, we show that PorB induces the condensation of the mitochondrial matrix and the loss of cristae structures, sensitizing cells to the induction of apoptosis via signaling pathways activated by BH3-only proteins. PorB is imported into mitochondria through the general translocase TOM but, unexpectedly, is not recognized by the SAM sorting machinery, usually required for the assembly of beta-barrel proteins in the mitochondrial outer membrane. PorB integrates into the mitochondrial inner membrane, leading to the breakdown of delta psi m. The PorB channel is regulated by nucleotides and an isogenic PorB mutant defective in ATP-binding failed to induce delta psi m loss and apoptosis, demonstrating that dissipation of delta psi m is a requirement for cell death caused by neisserial infection. Y1 - 2009 UR - http://publikationen.ub.uni-frankfurt.de/frontdoor/index/index/docId/22674 UR - https://nbn-resolving.org/urn:nbn:de:hebis:30-105273 SN - 1553-7374 N1 - Copyright: © 2009 Kozjak-Pavlovic et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. VL - 5 IS - (10): e1000629 PB - PLoS CY - Lawrence, Kan. ER -