Expression patterns of genes induced by oxidative stress in Porphyromonas gingivalis.
BACKGROUND
Porphyromonas gingivalis, a gram-negative anaerobic bacterium, is a major periopathogen whose transmission from host to host involves exposure to atmospheric oxygen. P. gingivalis contains genetic factors that function in an oxidative stress response, but their expression has not been analyzed during exposure to atmospheric oxygen. The aim of this study was to obtain a better understanding of atmospheric adaptation of P. gingivalis.


METHODS
The aerotolerance of wild-type and oxyR mutant P. gingivalis strains were determined, and quantitative polymerase chain reaction was performed to analyze gene expression patterns in response to exposure to atmospheric oxygen. The analyzed P. gingivalis genes encoded proteins involved in oxidative response (oxyR, ahpC-F, batA, dps, ftn, tpx) as well as several major virulence factors (hagA, hagB, hagE, rgpA, rgpB, hem).


RESULTS
Our results demonstrated a critical role for the oxyR gene in the aerotolerance of P. gingivalis. The ahpC-F, batA, and hem genes were slightly overexpressed (between 1.65-fold and 2-fold) after exposure to atmospheric oxygen compared to anaerobic conditions. The level of transcription of dps, ftn, tpx, and rgpA genes increased more than 2.5-fold, and the expression of ahpC-F, dps, ftn, and tpx was partially or completely OxyR-dependent.


CONCLUSIONS
A different transcription pattern of P. gingivalis genes was observed, depending on the stimulus of oxidative stress. We present new evidence that the expression of tpx, encoding a thiol peroxidase, is partially OxyR-dependent and is induced after atmospheric oxygen exposure.
Meuric
V
V
Université Européenne de Bretagne, Rennes Cedex, France.
Gracieux
P
P
Tamanai-Shacoori
Z
Z
Perez-Chaparro
J
J
Bonnaure-Mallet
M
M
D000222:Adaptation, Physiological / Q000235:genetics; D018829:Adhesins, Bacterial / Q000235:genetics; D000332:Aerobiosis / Q000235:genetics; D000693:Anaerobiosis / Q000235:genetics; D001426:Bacterial Proteins / Q000235:genetics; D003546:Cysteine Endopeptidases / Q000235:genetics; D004268:DNA-Binding Proteins / Q000235:genetics; D005293:Ferritins / Q000235:genetics; D015964:Gene Expression Regulation, Bacterial / Q000235:genetics*; D020868:Gene Silencing; D000080867:Gingipain Cysteine Endopeptidases; D006388:Hemagglutinins / Q000235:genetics; D006460:Hemolysin Proteins / Q000235:genetics; D006801:Humans; D009154:Mutation / Q000235:genetics; D018384:Oxidative Stress / Q000235:genetics*; D010544:Peroxidases / Q000235:genetics; D054464:Peroxiredoxins / Q000235:genetics; D016966:Porphyromonas gingivalis / Q000235:genetics*; D012329:RNA, Bacterial / Q000235:genetics; D012336:RNA, Ribosomal, 16S / Q000235:genetics; D014157:Transcription Factors / Q000235:genetics; D014774:Virulence / Q000235:genetics
D018829:Adhesins, Bacterial; D001426:Bacterial Proteins; D004268:DNA-Binding Proteins; C083911:DPS protein, Bacteria; D000080867:Gingipain Cysteine Endopeptidases; D006388:Hemagglutinins; D006460:Hemolysin Proteins; C530740:OxyR protein, P gingivalis; D012329:RNA, Bacterial; D012336:RNA, Ribosomal, 16S; D014157:Transcription Factors; D005293:Ferritins; D010544:Peroxidases; D054464:Peroxiredoxins; D003546:Cysteine Endopeptidases