VimA mediates multiple functions that control virulence in Porphyromonas gingivalis

Summary Porphyromonas gingivalis, a black‐pigmented, gram‐negative anaerobe, is an important etiological agent of periodontal disease. Its ability to survive in the periodontal pocket and orchestrate the microbial/host activities that can lead to disease suggest that P. gingivalis possesses a complex regulatory network involving transcriptional and post‐transcriptional mechanisms. The vimA (virulence modulating) gene is part of the 6.15‐kb bcp‐recA‐vimA‐vimE‐vimF‐aroG locus and plays a role in oxidative stress resistance. In addition to the glycosylation and anchorage of several surface proteins including the gingipains, VimA can also modulate sialylation, acetyl coenzyme A transfer, lipid A and its associated proteins and may be involved in protein sorting and transport. In this review, we examine the multifunctional role of VimA and discuss its possible involvement in a major regulatory network important for survival and virulence regulation in P. gingivalis. It is postulated that the multifunction of VimA is modulated via a post‐translational mechanism involving acetylation.