Publication Date:
2004-12-04
Description:
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.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ogawa, Michinaga -- Yoshimori, Tamotsu -- Suzuki, Toshihiko -- Sagara, Hiroshi -- Mizushima, Noboru -- Sasakawa, Chihiro -- New York, N.Y. -- Science. 2005 Feb 4;307(5710):727-31. Epub 2004 Dec 2.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology and Immunology, Institute of Medical Science, University of Tokyo, 4-6-1, Shirokanedai, Minato-ku, Tokyo 108-8639, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/15576571" target="_blank"〉PubMed〈/a〉
Keywords:
Animals
;
*Autophagy
;
Bacterial Proteins/genetics/*metabolism
;
Cell Line
;
DNA-Binding Proteins/*metabolism
;
Humans
;
Mice
;
Mice, Knockout
;
Microscopy, Electron
;
Microtubule-Associated Proteins/metabolism
;
Phagosomes/metabolism/*microbiology/ultrastructure
;
Protein Binding
;
Recombinant Fusion Proteins/metabolism
;
Shigella flexneri/genetics/growth & development/metabolism/*pathogenicity
;
Transcription Factors/*metabolism
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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