Quorum Sensing N-acyl Homoserine Lactones-SdiA Suppresses Escherichia coli-Pseudomonas aeruginosa Conjugation through Inhibiting traI Expression

Abstract

Conjugation is a key mechanism for horizontal gene transfer and plays an important role in bacterial evolution, especially with respect to antibiotic resistance. However, little is known about the role of donor and recipient cells in regulation of conjugation. Here, using an <i>Escherichia coli</i> (<i>SM10</i>λπ)-<i>Pseudomonas aeruginosa</i> (<i>PAO1</i>) conjugation model, we demonstrated that deficiency of <i>lasI</i>/<i>rhlI</i>, genes associated with generation of the quorum sensing signals N-acyl homoserine lactones (AHLs) in <i>PAO1</i>, or deletion of the AHLs receptor SdiA in the donor <i>SM10</i>λπ both facilitated conjugation. When using another AHLs-non-producing <i>E. coli</i> strain <i>EC600</i> as recipient cells, deficiency of <i>sdiA</i> in donor <i>SM10</i>λπ hardly affect the conjugation. More importantly, in the presence of exogenous AHLs, the conjugation efficiency between <i>SM10</i>λπ and <i>EC600</i> was dramatically decreased, while deficiency of <i>sdiA</i> in <i>SM10</i>λπ attenuated AHLs-inhibited conjugation. These data suggest the conjugation suppression function of AHLs-SdiA chemical signaling. Further bioinformatics analysis, β-galactosidase reporter system and electrophoretic mobility shift assays characterized the binding site of SdiA on the promoter region of <i>traI</i> gene. Furthermore, deletion of <i>lasI</i>/<i>rhlI</i> or <i>sdiA</i> promoted <i>traI</i> mRNA expression in <i>SM10</i>λπ and <i>PAO1</i> co-culture system, which was abrogated by AHLs. Collectively, our results provide new insight into an important contribution of quorum sensing system AHLs-SdiA to the networks that regulate conjugation.