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Neisserial porin (PorB) causes rapid calcium influx in target cells and induces apoptosis by the activation of cysteine proteases
Author(s) -
Müller Anne,
Günther Dirk,
Düx Frank,
Naumann Michael,
Meyer Thomas F.,
Rudel Thomas
Publication year - 1999
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/18.2.339
Subject(s) - biology , proteases , porin , cysteine , apoptosis , biochemistry , calcium , microbiology and biotechnology , enzyme , bacterial outer membrane , gene , escherichia coli , medicine
The porin (PorB) of Neisseria gonorrhoeae is an intriguing bacterial factor owing to its ability to translocate from the outer bacterial membrane into host cell membranes where it modulates the infection process. Here we report on the induction of programmed cell death after prolonged infection of epithelial cells with pathogenic Neisseria species. The underlying mechanism we propose includes translocation of the porin, a transient increase in cytosolic Ca 2+ and subsequent activation of the Ca 2+ dependent protease calpain as well as proteases of the caspase family. Blocking the porin channel by ATP eliminates the Ca 2+ signal and also abolishes its pro‐apoptotic function. The neisserial porins share structural and functional homologies with the mitochondrial voltage‐dependent anion channels (VDAC). The neisserial porin may be an analogue or precursor of the ancient permeability transition pore, the putative central regulator of apoptosis.