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Characterization of a Brucella abortus mutant defective for the association with endoplasmic reticulum exit sites in HeLa cells.
MedLine Citation:
PMID:  22820839     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Brucellae are facultative intracellular pathogenic bacteria able to control maturation of their vacuoles. In several cell types, Brucella is able to reach a proliferation compartment derived from the endoplasmic reticulum (ER). Since ER exit site (ERES) functions are required for Brucella proliferation, we performed a yeast two-hybrid screen between human ERES associated proteins and the predicted Brucella proteome. This screening led to the identification of CstA, a conserved protein that specifically interacts with Sec24A, a component of the ERES. We found that a tagged CstA is secreted in Brucella abortus culture medium. This secretion is independent of the type IV secretion system VirB and the flagellum, suggesting that CstA is secreted through another system. We also discovered that a B. abortus cstA mutant is impaired for its association with the Sec23 ERES marker. The B. abortus cstA mutant displayed peculiar trafficking, with reduced association with LAMP1 and Calnexin at 12 h post-infection in HeLa cells. However, its intracellular proliferation kinetics was not affected. The data reported here suggest that CstA could be directly or indirectly involved in the control of B. abortus intracellular trafficking in HeLa cells.
Authors:
Marie de Barsy; Aurélie Mirabella; Jean-Jacques Letesson; Xavier De Bolle
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2012-7-19
Journal Detail:
Title:  Microbiology (Reading, England)     Volume:  -     ISSN:  1465-2080     ISO Abbreviation:  -     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-7-23     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9430468     Medline TA:  Microbiology     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Affiliation:
University of Namur (FUNDP).
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