The small FNR regulon of Neisseria gonorrhoeae: comparison with the larger Escherichia coli FNR regulon and interaction with the NarQ-NarP regulon

Abstract

Background: Neisseria gonorrhoeae can survive during oxygen starvation by reducing nitrite to nitrous oxide catalysed by the nitrite and nitric oxide reductases, AniA and NorB. The oxygen-sensing transcription factor, FNR, is essential for transcription activation at the aniA promoter, and full activation also requires the twocomponent regulatory system, NarQ-NarP, and the presence of nitrite. The only other gene known to be activated by the gonococcal FNR is ccp encoding a cytochrome c peroxidase, and no FNR-repressed genes have been reported in the gonococcus. In contrast, FNR acts as both an activator and repressor involved in the control of more than 100 operons in E. coli regulating major changes in the adaptation from aerobic to anaerobic conditions. In this study we have performed a microarray-led investigation of the FNR-mediated responses in N. gonorrhoeae to determine the physiological similarities and differences in the role of FNR in cellular regulation in this species.

Speed Switching of Gonococcal Surface Motility Correlates with Proton Motive Force

“…Twitching motility assays revealed that the time point of global switching was unchanged. This was expected because denitrification must be induced by the oxygen-sensing transcription factor FNR [26] [29]. We did not observe a global switching back to the high speed mode even 60 min after the first global switching event, indicating that the denitrification pathway does not show a major influence on oxygen-dependent speed switching.…”

“…This was expected because denitrification must be induced by the oxygen-sensing transcription factor FNR [26] [29]. Although a few minutes after global switching a very small fraction of bacteria (< 5%) showed a twitching speed almost comparable to the high speed mode under aerobic conditions, addition of nitrite did not induce a back-switch of the population to the high speed mode within 1h after oxygen depletion.…”

Esterase D Is Essential for Protection ofNeisseria gonorrhoeaeagainst Nitrosative Stress and for Bacterial Growth during Interaction with Cervical Epithelial Cells

“…In a recent study, we showed that NmlR-regulated trxB, which encodes thioredoxin reductase, is required to confer protection of N. gonorrhoeae against killing by NO, and our data indicate that TrxB is required to maintain a high level of expression of aniA and norB [7]. NmlR itself is under the control of Fnr [13]; therefore, a role for the NmlR regulon in the anaerobic physiology of the gonococcus is not unexpected. The data presented in this report indicate that another NmlR-regulated gene, estD , is also required for defense of N. gonorrhoeae against nitrosative stress.…”

Characterization of an ntrX Mutant of Neisseria gonorrhoeae Reveals a Response Regulator That Controls Expression of Respiratory Enzymes in Oxidase-Positive Proteobacteria

“…Our observation that NADH dehydrogenase and pyridine nucleotide transhydrogenase activities were also affected by the mutation in R. capsulatus ntrX suggests that the NtrYX TCS may have a substantive effect on wider bioenergetic functions in R. capsulatus. FNR has been shown to also regulate cco and aniA expression in N. gonorrhoeae (66). The NarPQ TCS and the repressor NsrR are also involved in the control of aniA expression as part of the partial (AniA-NorB) denitrification pathway in N. gonorrhoeae (67).…”