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Comparison of the RpoH-dependent regulon and general stress response in Neisseria gonorrhoeae.

ABSTRACT: In the gammaproteobacteria the RpoH regulon is often equated with the stress response, as the regulon contains many of the genes that encode what have been termed heat shock proteins that deal with the presence of damaged proteins. However, the betaproteobacteria primarily utilize the HrcA repressor protein to control genes involved in the stress response. We used genome-wide transcriptional profiling to compare the RpoH regulon and stress response of Neisseria gonorrhoeae, a member of the betaproteobacteria. To identify the members of the RpoH regulon, a plasmid-borne copy of the rpoH gene was overexpressed during exponential-phase growth at 37 degrees C. This resulted in increased expression of 12 genes, many of which encode proteins that are involved in the stress response in other species. The putative promoter regions of many of these up-regulated genes contain a consensus RpoH binding site similar to that of Escherichia coli. Thus, it appears that unlike other members of the betaproteobacteria, N. gonorrhoeae utilizes RpoH, and not an HrcA homolog, to regulate the stress response. In N. gonorrhoeae exposed to 42 degrees C for 10 min, we observed a much broader transcriptional response involving 37 differentially expressed genes. Genes that are apparently not part of the RpoH regulon showed increased transcription during heat shock. A total of 13 genes were also down-regulated. From these results we concluded that although RpoH acts as the major regulator of protein homeostasis, N. gonorrhoeae has additional means of responding to temperature stress.

SUBMITTER: Gunesekere IC

PROVIDER: S-EPMC1483004 | biostudies-literature | 2006 Jul

REPOSITORIES: biostudies-literature

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Comparison of the RpoH-dependent regulon and general stress response in Neisseria gonorrhoeae.

Gunesekere Ishara C IC Kahler Charlene M CM Powell David R DR Snyder Lori A S LA Saunders Nigel J NJ Rood Julian I JI Davies John K JK

Journal of bacteriology 20060701 13

In the gammaproteobacteria the RpoH regulon is often equated with the stress response, as the regulon contains many of the genes that encode what have been termed heat shock proteins that deal with the presence of damaged proteins. However, the betaproteobacteria primarily utilize the HrcA repressor protein to control genes involved in the stress response. We used genome-wide transcriptional profiling to compare the RpoH regulon and stress response of Neisseria gonorrhoeae, a member of the betap ...[more]

PMID: 16788186

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Project description:BackgroundNeisseria 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 two-component 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.ResultsMicroarray experiments show that N. gonorrhoeae FNR controls a much smaller regulon than its E. coli counterpart; it activates transcription of aniA and thirteen other genes, and represses transcription of six genes that include dnrN and norB. Having previously shown that a single amino acid substitution is sufficient to enable the gonococcal FNR to complement an E. coli fnr mutation, we investigated whether the gonococcal NarQ-NarP can substitute for E. coli NarX-NarL or NarQ-NarP. A plasmid expressing gonococcal narQ-narP was unable to complement E. coli narQP or narXL mutants, and was insensitive to nitrate or nitrite. Mutations that progressively changed the periplasmic nitrate sensing region, the P box, of E. coli NarQ to the sequence of the corresponding region of gonococcal NarQ resulted in loss of transcription activation in response to the availability of either nitrate or nitrite. However, the previously reported ligand-insensitive ability of gonococcal NarQ, the "locked on" phenotype, to activate either E. coli NarL or NarP was confirmed.ConclusionDespite the sequence similarities between transcription activators of E. coli and N. gonorrhoeae, these results emphasise the fundamental differences in transcription regulation between these two types of pathogenic bacteria.

Dataset Information

Comparison of the RpoH-dependent regulon and general stress response in Neisseria gonorrhoeae.

Publications

Comparison of the RpoH-dependent regulon and general stress response in Neisseria gonorrhoeae.

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