Premium
Two pKM101‐encoded proteins, the pilus‐tip protein TraC and Pep, assemble on the Escherichia coli cell surface as adhesins required for efficient conjugative DNA transfer
Author(s) -
GonzálezRivera Christian,
Khara Pratick,
Awad Dominik,
Patel Roosheel,
Li Yang Grace,
Bogisch Maxim,
Christie Peter J.
Publication year - 2019
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.14141
Subject(s) - pilus , biology , bacterial conjugation , secretion , trac , type vi secretion system , microbiology and biotechnology , bacterial adhesin , complementation , cell envelope , escherichia coli , transport protein , biofilm , extracellular , dna , plasmid , genetics , bacteria , biochemistry , virulence , gene , phenotype , computer science , programming language
Summary Mobile genetic elements (MGEs) encode type IV secretion systems (T4SSs) known as conjugation machines for their transmission between bacterial cells. Conjugation machines are composed of an envelope‐spanning translocation channel, and those functioning in Gram‐negative species additionally elaborate an extracellular pilus to initiate donor‐recipient cell contacts. We report that pKM101, a self‐transmissible MGE functioning in the Enterobacteriaceae , has evolved a second target cell attachment mechanism. Two pKM101‐encoded proteins, the pilus‐tip adhesin TraC and a protein termed Pep, are exported to the cell surface where they interact and also form higher order complexes appearing as distinct foci or patches around the cell envelope. Surface‐displayed TraC and Pep are required for an efficient conjugative transfer, ‘extracellular complementation’ potentially involving intercellular protein transfer, and activation of a Pseudomonas aeruginosa type VI secretion system. Both proteins are also required for bacteriophage PRD1 infection. TraC and Pep are exported across the outer membrane by a mechanism potentially involving the β‐barrel assembly machinery. The pKM101 T4SS, thus, deploys alternative routing pathways for the delivery of TraC to the pilus tip or both TraC and Pep to the cell surface. We propose that T4SS‐encoded, pilus‐independent attachment mechanisms maximize the probability of MGE propagation and might be widespread among this translocation superfamily.