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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.

the journal of infectious diseases (online. university of chicago press)/the journal of infectious diseases

Comparative Analysis of Type III Effector Translocation by<i>Yersinia pseudotuberculosis</i>Expressing Native LcrV or PcrV from<i>Pseudomonas aeruginosa</i>

Comparative Analysis of Type III Effector Translocation byYersinia pseudotuberculosisExpressing Native LcrV or PcrV fromPseudomonas aeruginosa