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Comparative Analysis of Type III Effector Translocation byYersinia pseudotuberculosisExpressing Native LcrV or PcrV fromPseudomonas aeruginosa
Author(s) -
Jeanette E. Bröms,
Charlotta Sundin,
Matthew S. Francis,
Åke Försberg
Publication year - 2003
Publication title -
the journal of infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.69
H-Index - 252
eISSN - 1537-6613
pISSN - 0022-1899
DOI - 10.1086/376452
Subject(s) - yersinia pseudotuberculosis , yersinia , microbiology and biotechnology , biology , effector , yersinia enterocolitica , chromosomal translocation , yersinia infections , complementation , pseudomonas aeruginosa , enterobacteriaceae , virulence , bacteria , escherichia coli , biochemistry , genetics , gene , mutant
The homologues LcrV of Yersinia species and PcrV of Pseudomonas aeruginosa are pore-forming components. When expressed in a Yersinia lcrV background, PcrV formed smaller pores in infected erythrocyte membranes, correlating to a lowered translocation of Yersinia effectors. To understand this phenomenon, cytotoxins exoenzyme S of P. aeruginosa and YopE of Yersinia were introduced into a Yersinia background without Yop effectors but expressing LcrV or PcrV. Comparable translocation of each substrate indicated that substrate recognition by LcrV/PcrV is not a regulator of translocation. Yersinia harboring pcrV coexpressed with its native operon efficiently translocated effectors into HeLa cell monolayers and formed large LcrV-like pores in erythrocyte membranes. Thus, a PcrV complex with native P. aeruginosa translocon components is required to form fully functional pores for complete complementation of effector translocation in Yersinia.

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