Quorum Sensing N-acyl Homoserine Lactones-SdiA SuppressesEscherichia coli-Pseudomonas aeruginosaConjugation through InhibitingtraIExpression.
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 anEscherichia coli(SM10λπ)-Pseudomonas aeruginosa(PAO1) conjugation model, we demonstrated that deficiency oflasI/rhlI, genes associated with generation of the quorum sensing signals N-acyl homoserine lactones (AHLs) inPAO1, or deletion of the AHLs receptor SdiA in the donorSM10λπ both facilitated conjugation. When using another AHLs-non-producingE. colistrainEC600as recipient cells, deficiency ofsdiAin donorSM10λπ hardly affect the conjugation. More importantly, in the presence of exogenous AHLs, the conjugation efficiency betweenSM10λπ andEC600was dramatically decreased, while deficiency ofsdiAinSM10λπ 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 oftraIgene. Furthermore, deletion oflasI/rhlIorsdiApromotedtraImRNA expression inSM10λπ andPAO1co-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.
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou, China; Postdoctoral Mobile Station, Guangzhou University of Chinese MedicineGuangzhou, China.
Yang
Y
Lu
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou, China.
Jianming
J
Zeng
The Second Clinical College, Guangzhou University of Chinese Medicine Guangzhou, China.
Binning
B
Wu
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou, China.
Shunmei
S
E
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou, China.
Lina
L
Wang
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou, China.
Renxin
R
Cai
Clinical Microbiology Laboratory, Guangdong Academy of Medical Science and Guangdong General Hospital Guangzhou, China.
Ni
N
Zhang
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou, China.
Youqiang
Y
Li
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese MedicineGuangzhou, China; Postdoctoral Mobile Station, Guangzhou University of Chinese MedicineGuangzhou, China.
Xianzhang
X
Huang
Department of Laboratory Medicine, The First Affiliated Hospital of Sun Yat-sen University Guangzhou, China.
Bin
B
Huang
Department of Laboratory Medicine, The Second Affiliated Hospital of Guangzhou University of Chinese Medicine Guangzhou, China.
Cha
C
Chen
D054742:Acyl-Butyrolactones / Q000378:metabolism*; D003227:Conjugation, Genetic / Q000187:drug effects*; D004265:DNA Helicases / Q000378:metabolism*; D004926:Escherichia coli / Q000187:drug effects* / Q000235:genetics*; D029968:Escherichia coli Proteins / Q000378:metabolism*; D015964:Gene Expression Regulation, Bacterial / Q000187:drug effects; D011550:Pseudomonas aeruginosa / Q000235:genetics*; D015534:Trans-Activators / Q000378:metabolism*
D054742:Acyl-Butyrolactones; D029968:Escherichia coli Proteins; D015534:Trans-Activators; C490806:sdiA protein, E coli; C027093:TraI protein, E coli; D004265:DNA Helicases
N-acyl homoserine lactones; P. aeruginosa; SdiA; antibiotic resistance; conjugation