Escape of intracellular Shigella from autophagy.
The degradation of undesirable cellular components or organelles, including invading microbes, by autophagy is crucial for cell survival. Here, Shigella, an invasive bacteria, was found to be able to escape autophagy by secreting IcsB by means of the type III secretion system. Mutant bacteria lacking IcsB were trapped by autophagy during multiplication within the host cells. IcsB did not directly inhibit autophagy. Rather, Shigella VirG, a protein required for intracellular actin-based motility, induced autophagy by binding to the autophagy protein, Atg5. In nonmutant Shigella, this binding is competitively inhibited by IcsB binding to VirG.
Ogawa
Michinaga
M
Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.
Yoshimori
Tamotsu
T
Suzuki
Toshihiko
T
Sagara
Hiroshi
H
Mizushima
Noboru
N
Sasakawa
Chihiro
C
D000818:Animals; D001343:Autophagy; D000071187:Autophagy-Related Protein 5; D001426:Bacterial Proteins / Q000235:genetics / Q000378:metabolism*; D002460:Cell Line; D004268:DNA-Binding Proteins / Q000378:metabolism*; D006801:Humans; D051379:Mice; D018345:Mice, Knockout; D008854:Microscopy, Electron; D008869:Microtubule-Associated Proteins / Q000378:metabolism; D010588:Phagosomes / Q000378:metabolism / Q000382:microbiology* / Q000648:ultrastructure; D011485:Protein Binding; D011993:Recombinant Fusion Proteins / Q000378:metabolism; D012763:Shigella flexneri / Q000235:genetics / Q000254:growth & development / Q000378:metabolism / Q000472:pathogenicity*; D014157:Transcription Factors / Q000378:metabolism*
C495773:Atg5 protein, mouse; D000071187:Autophagy-Related Protein 5; D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; D008869:Microtubule-Associated Proteins; D011993:Recombinant Fusion Proteins; D014157:Transcription Factors; C058483:virG protein, Shigella flexneri