Micro-managing the executioner: pathogen targeting of mitochondria.
Eukaryotic cell viability is largely regulated at the level of mitochondria, with cell death executed by endogenous proteins that act to increase the permeability of the inner and/or outer membranes of these organelles. The gastric pathogen, Helicobacter pylori, can mimic this mechanism by producing the pro-apoptotic toxin, VacA, which was recently demonstrated to (i) localize to mitochondria within epithelial cells, (ii) rapidly transport into mitochondria in vitro, and (iii) induce changes consistent with permeabilization of mitochondrial membranes by a mechanism dependent on cellular entry and toxin membrane channel activity. The targeting of mitochondrial membranes is emerging as a strategy used by pathogenic microbes to control cell viability while circumventing upstream pathways and checkpoints of cell death.
Blanke
Steven R
SR
Department of Microbiology and Molecular Genetics, University of Illinois, 302 Burrill Hall, Urbana-Champaign, IL 61801, USA. sblanke@uh.edu
D017209:Apoptosis / Q000502:physiology*; D001426:Bacterial Proteins / Q000502:physiology; D002462:Cell Membrane / Q000382:microbiology / Q000502:physiology; D016481:Helicobacter Infections / Q000382:microbiology*; D016480:Helicobacter pylori / Q000472:pathogenicity / Q000502:physiology*; D006801:Humans; D008928:Mitochondria / Q000382:microbiology* / Q000502:physiology*
D001426:Bacterial Proteins; C074689:VacA protein, Helicobacter pylori