Abstract
Porphyromonas gingivalis is a late-colonizing bacterium of the subgingival dental plaque biofilm associated with periodontitis. Two P. gingivalis genes, fimR and fimS, are predicted to encode a two-component signal transduction system comprising a response regulator (FimR) and a sensor histidine kinase (FimS). In this study, we show that fimS and fimR, although contiguous on the genome, are not part of an operon. We inactivated fimR and fimS in both the afimbriated strain W50 and the fimbriated strain ATCC 33277 and demonstrated that both mutants formed significantly less biofilm than their respective wild-type strains. Quantitative reverse transcription-real-time PCR showed that expression of fimbriation genes was reduced in both the fimS and fimR mutants of strain ATCC 33277. The mutations had no effect, in either strain, on the P. gingivalis growth rate or on the response to hydrogen peroxide or growth at pH 9, at 41 degrees C, or at low hemin availability. Transcriptome analysis using DNA microarrays revealed that inactivation of fimS resulted in the differential expression of 10% of the P. gingivalis genome (>1.5-fold; P < 0.05). Notably genes encoding seven different transcriptional regulators, including the fimR gene and three extracytoplasmic sigma factor genes, were differentially expressed in the fimS mutant.