Re-use of this article is permitted in accordance with the Creative Commons Deed, Attribution 2.5, which does not permit commercial exploitation.
A new Vibrio cholerae sRNA modulates colonization and affects release of outer membrane vesicles
Article first published online: 4 AUG 2008
© 2008 The Authors. Journal compilation © 2008 Blackwell Publishing Ltd
Volume 70, Issue 1, pages 100–111, October 2008
How to Cite
Song, T., Mika, F., Lindmark, B., Liu, Z., Schild, S., Bishop, A., Zhu, J., Camilli, A., Johansson, J., Vogel, J. and Wai, S. N. (2008), A new Vibrio cholerae sRNA modulates colonization and affects release of outer membrane vesicles. Molecular Microbiology, 70: 100–111. doi: 10.1111/j.1365-2958.2008.06392.x
- Issue published online: 11 SEP 2008
- Article first published online: 4 AUG 2008
- Accepted 27 July, 2008.
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, σE, 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.