Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 15 February 2011
Vol. 4, Issue 160, p. ec52
[DOI: 10.1126/scisignal.4160ec52]


Microbiology Deadly Switch

Stella M. Hurtley

Science, AAAS, Cambridge CB2 1LQ, UK

Numerous bacterial species, such as Neisseria meningitidis, thrive in the mouth, throat, and gut, or on the skin, and propagate from one host to the next. Most of the time, cohabitation with these commensals has no pathological consequences and can even be beneficial. However, commensal species are occasionally responsible for severe invasive infections, including septicemia and meningitis. Chamot-Rooke et al. describe the details of a molecular switch that takes place during the infection cycle of N. meningitidis that allows it to disseminate. The process depends on a regulated posttranslational modification of the N. meningitidis pilin, the major component of a filamentous adhesive structure, the type IV pilus. This modification caused bacteria to maintain their adhesive properties to the host cell surface but to lose their ability to stay attached to bacterial microcolonies, so that a small proportion of bacteria are thus free to colonize new hosts and propagate.

J. Chamot-Rooke, G. Mikaty, C. Malosse, M. Soyer, A. Dumont, J. Gault, A.-F. Imhaus, P. Martin, M. Trellet, G. Clary, P. Chafey, L. Camoin, M. Nilges, X. Nassif, G. Duménil, Posttranslational modification of pili upon cell contact triggers N. meningitidis dissemination. Science 331, 778–782 (2011). [Abstract] [Full Text]

Citation: S. M. Hurtley, Deadly Switch. Sci. Signal. 4, ec52 (2011).

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882