Document Detail


The extreme C terminus of Shigella flexneri IpaB is required for regulation of type III secretion, needle tip composition, and binding.
MedLine Citation:
PMID:  20086081     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Type III secretion systems (T3SSs) are widely distributed virulence determinants of Gram-negative bacteria. They translocate bacterial proteins into host cells to manipulate them during infection. The Shigella T3SS consists of a cytoplasmic bulb, a transmembrane region, and a hollow needle protruding from the bacterial surface. The distal tip of mature, quiescent needles is composed of IpaD, which is topped by IpaB. Physical contact with host cells initiates secretion and leads to assembly of a pore, formed by IpaB and IpaC, in the host cell membrane, through which other virulence effector proteins may be translocated. IpaB is required for regulation of secretion and may be the host cell sensor. However, its mode of needle association is unknown. Here, we show that deletion of 3 or 9 residues at the C terminus of IpaB leads to fast constitutive secretion of late effectors, as observed in a DeltaipaB strain. Like the DeltaipaB mutant, mutants with C-terminal mutations also display hyperadhesion. However, unlike the DeltaipaB mutant, they are still invasive and able to lyse the internalization vacuole with nearly wild-type efficiency. Finally, the mutant proteins show decreased association with needles and increased recruitment of IpaC. Taken together, these data support the notion that the state of the tip complex regulates secretion. We propose a model where the quiescent needle tip has an "off" conformation that turns "on" upon host cell contact. Our mutants may adopt a partially "on" conformation that activates secretion and is capable of recruiting some IpaC to insert pores into host cell membranes and allow invasion.
Authors:
A Dorothea Roehrich; Isabel Martinez-Argudo; Steven Johnson; Ariel J Blocker; Andreas K J Veenendaal
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-01-19
Journal Detail:
Title:  Infection and immunity     Volume:  78     ISSN:  1098-5522     ISO Abbreviation:  Infect. Immun.     Publication Date:  2010 Apr 
Date Detail:
Created Date:  2010-03-17     Completed Date:  2010-04-16     Revised Date:  2014-02-19    
Medline Journal Info:
Nlm Unique ID:  0246127     Medline TA:  Infect Immun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1682-91     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Bacterial Adhesion
Bacterial Proteins / genetics*,  metabolism*
Gene Deletion
Humans
Membrane Transport Proteins / genetics*,  metabolism*
Models, Biological
Mutant Proteins / genetics,  metabolism
Protein Binding
Protein Interaction Mapping
Sequence Deletion
Shigella flexneri / pathogenicity*
Virulence Factors / genetics*,  metabolism*
Grant Support
ID/Acronym/Agency:
082398//Wellcome Trust; G0400389//Medical Research Council; G0401595//Medical Research Council; G0701243//Medical Research Council
Chemical
Reg. No./Substance:
0/Bacterial Proteins; 0/Membrane Transport Proteins; 0/Mutant Proteins; 0/Virulence Factors; 127384-62-7/ipaB protein, Shigella
Comments/Corrections

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