A new Vibrio cholerae sRNA modulates colonization and affects release of outer membrane vesicles |
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Authors: | Song Tianyan Mika Franziska Lindmark Barbro Liu Zhi Schild Stefan Bishop Anne Zhu Jun Camilli Andrew Johansson Jörgen Vogel Jörg Wai Sun Nyunt |
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Affiliation: | 1. Department of Molecular Biology, Ume? University, SE‐901 87 Ume?, Sweden.;2. RNA Biology Group, Max Planck Institute for Infection Biology, 10117 Berlin, Germany.;3. Departments of Microbiology, Physics, and Biology, University of Pennsylvania, Philadelphia, PA 19104, USA.;4. Howard Hughes Medical Institute and the Department of Molecular Biology an Microbiology, Tufts University School of Medicine, Boston, MA 02111, USA. |
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Abstract: | We discovered a new small non-coding RNA (sRNA) gene, vrrA of Vibrio cholerae O1 strain A1552. A vrrA mutant overproduces OmpA porin, and we demonstrate that the 140 nt VrrA RNA represses ompA translation by base-pairing with the 5' region of the mRNA. The RNA chaperone Hfq is not stringently required for VrrA action, but expression of the vrrA gene requires the membrane stress sigma factor, sigma(E), suggesting that VrrA acts on ompA in response to periplasmic protein folding stress. We also observed that OmpA levels inversely correlated with the number of outer membrane vesicles (OMVs), and that VrrA increased OMV production comparable to loss of OmpA. VrrA is the first sRNA known to control OMV formation. Moreover, a vrrA mutant showed a fivefold increased ability to colonize the intestines of infant mice as compared with the wild type. There was increased expression of the main colonization factor of V. cholerae, the toxin co-regulated pili, in the vrrA mutant as monitored by immunoblot detection of the TcpA protein. VrrA overproduction caused a distinct reduction in the TcpA protein level. Our findings suggest that VrrA contributes to bacterial fitness in certain stressful environments, and modulates infection of the host intestinal tract. |
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