Antagonistic self-sensing and mate-sensing signaling controls antibiotic-resistance transfer
Antagonistic self-sensing and mate-sensing signaling controls antibiotic-resistance transfer
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DOI:
10.1073/pnas.1212256110
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发表时间:
2013-04-23
影响因子:
11.1
通讯作者:
Hu, Wei-Shou
中科院分区:
文献类型:
--
作者:
Chatterjee, Anushree;Cook, Laura C. C.;Hu, Wei-Shou
Conjugation is one of the most common ways bacteria acquire antibiotic resistance, contributing to the emergence of multidrug-resistant "superbugs." Bacteria of the genus Enterococcus faecalis are highly antibiotic-resistant nosocomial pathogens that use the mechanism of conjugation to spread antibiotic resistance between resistance-bearing donor cells and resistance-deficient recipient cells. Here, we report a unique quorum sensing-based communication system that uses two antagonistic signaling molecules to regulate conjugative transfer of tetracycline-resistance plasmid pCF10 in E. faecalis. A "mate-sensing" peptide sex pheromone produced by recipient cells is detected by donor cells to induce conjugative genetic transfer. Using mathematical modeling and experimentation, we show that a second antagonistic "self-sensing" signaling peptide, previously known to suppress self-induction of donor cells, also serves as a classic quorum-sensing signal for donors that functions to reduce antibiotic-resistance transfer at high donor density. This unique form of quorum sensing may provide a means of limiting the spread of the plasmid and present opportunities to control antibiotic-resistance transfer through manipulation of intercellular signaling, with implications in the clinical setting.