Gonococcal nitric oxide reductase is encoded by a single gene, norB, whichis required for anaerobic growth and is induced by nitric oxide

Citation
Tc. Householder et al., Gonococcal nitric oxide reductase is encoded by a single gene, norB, whichis required for anaerobic growth and is induced by nitric oxide, INFEC IMMUN, 68(9), 2000, pp. 5241-5246
Citations number
34
Categorie Soggetti
Immunology
Journal title
INFECTION AND IMMUNITY
ISSN journal
00199567 → ACNP
Volume
68
Issue
9
Year of publication
2000
Pages
5241 - 5246
Database
ISI
SICI code
0019-9567(200009)68:9<5241:GNORIE>2.0.ZU;2-I
Abstract
The gene encoding a nitric oxide reductase has been identified in Neisseria gonorrhoeae. The norB gene product shares significant identity with the ni tric oxide reductases in Ralstonia eutropha and Synechocystis sp, and, like those organisms, the gonococcus lacks a norC homolog. The gonococcal norB gene was found to be required for anaerobic growth, but the absence of norB did not dramatically decrease anaerobic survival. In a wild-type backgroun d, induction of norB expression was seen anaerobically in the presence of n itrite but not anaerobically without nitrite or aerobically. norB expressio n is not regulated by FNR or NarP, but a functional aniA gene (which encode s an anaerobically induced outer membrane nitrite reductase) is necessary f or expression, When aniA is constitutively expressed, norB expression can b e induced both anaerobically and aerobically, but only in the presence of n itrite, suggesting that nitric oxide, which is likely to be produced by Ani A as a product of nitrite reduction, is the inducing agent. This was confir med with the use of the nitric oxide donor, spermine-nitric oxide complex, in an aniA null background both anaerobically and aerobically. NorB is impo rtant for gonococcal adaptation to an anaerobic environment, a physiologica lly relevant state during gonococcal infection. The presence of this enzyme , which is induced by nitric oxide, may also have implications in immune ev asion and immunomodulation in the human host.