Document Detail


IpaD of Shigella flexneri is independently required for regulation of Ipa protein secretion and efficient insertion of IpaB and IpaC into host membranes.
MedLine Citation:
PMID:  15731041     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Shigella flexneri causes human dysentery after invading the cells of the colonic epithelium. The best-studied effectors of Shigella entry into colonocytes are the invasion plasmid antigens IpaC and IpaB. These proteins are exported via a type III secretion system (TTSS) to form a pore in the host membrane that may allow the translocation of other effectors into the host cytoplasm. TTSS-mediated secretion of IpaD is also required for translocation pore formation, bacterial invasion, and virulence, but the mechanistic role of this protein is unclear. IpaD is also known to be involved in controlling Ipa protein secretion, but here it is shown that this activity can be separated from its requirement for cellular invasion. Amino acids 40 to 120 of IpaD are not essential for IpaD-dependent invasion; however, deletions in this region still lead to constitutive IpaB/IpaC secretion. Meanwhile, a central deletion causes only a partial loss of control of Ipa secretion but completely eliminates IpaD's invasion function, indicating that IpaD's role in invasion is not a direct outcome of its ability to control Ipa secretion. As shigellae expressing ipaD N-terminal deletion mutations have reduced contact-mediated hemolysis activity and are less efficient at introducing IpaB and IpaC into erythrocyte membranes, it is possible that IpaD is responsible for insertion of IpaB/IpaC pores into target cell membranes. While efficient insertion of IpaB/IpaC pores is needed for optimal invasion efficiency, it may be especially important for Ipa-dependent membrane disruption and thus for efficient vacuolar escape and intercellular spread.
Authors:
Wendy L Picking; Hiroaki Nishioka; Patricia D Hearn; M Aaron Baxter; Amanda T Harrington; Ariel Blocker; William D Picking
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Infection and immunity     Volume:  73     ISSN:  0019-9567     ISO Abbreviation:  Infect. Immun.     Publication Date:  2005 Mar 
Date Detail:
Created Date:  2005-02-25     Completed Date:  2005-04-01     Revised Date:  2013-10-31    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1432-40     Citation Subset:  IM    
Affiliation:
Department of Molecular Biosciences, University of Kansas, 1200 Sunnyside Ave., Lawrence, KS 66045, USA. picking@ku.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, Bacterial / genetics,  metabolism*
Bacterial Proteins / genetics,  metabolism*
Cell Line
Cell Membrane / metabolism*
Erythrocyte Membrane / metabolism,  microbiology
Gene Deletion
Gene Expression Regulation, Bacterial*
Hemolysis
Humans
Intestines / cytology,  microbiology
Shigella flexneri / genetics,  metabolism,  pathogenicity*
Grant Support
ID/Acronym/Agency:
AI034428/AI/NIAID NIH HHS; K22 AI01847/AI/NIAID NIH HHS; P20 RR017708-03/RR/NCRR NIH HHS; R01 AI034428/AI/NIAID NIH HHS; RR017708/RR/NCRR NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, Bacterial; 0/Bacterial Proteins; 0/IpaD protein, Shigella flexneri; 127384-62-7/ipaB protein, Shigella; 127384-63-8/IpaC protein, Shigella
Comments/Corrections

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