Abstract

Our understanding of how oral microbiota adapt in response to changes in their surroundings remains limited. This is particularly true of the slow-growing anaerobes that persist below the gum line. Here, we report that the oral anaerobe Porphyromonas gingivalis strain 381 can surface translocate when sandwiched between two surfaces. We show that during movement, this bacterium alters its metabolism, specifically side products of arginine utilization including citrulline and ornithine accumulated in the translocating cells; while arginine, N-acetyl-arginine, and the polyamine putrescine, which is produced from arginine were consumed. In addition, our results indicate that movement requires modification of the surrounding environment via proteolysis, cell dispersion, cell-on-cell rolling, and sub-diffusive cell-driven motility. We also show that production of fimbriae and fimbriae-associated proteins; as well as the regulation of contact-dependent growth inhibition genes, which are known to be involved in self-nonself discrimination, and the type IX secretion system are central to surface translocation. These studies provide a first glimpse into P. gingivalis motility and its relationship to ecological variables.

Highlights

  • Porphyromonas gingivalis is strongly implicated in the onset and progression of periodontitis, a chronic inflammatory disease of the gingival tissues with systemic impact on human health [1,2,3,4]

  • The results presented here demonstrate an as yet unreported surface motility for P. gingivalis historically known as a sessile, non-motile bacterium

  • contact-dependent growth inhibition (CDI) is a ubiquitous mechanism that plays a key role in competition strategies, via delivery of toxins that kills neighboring target bacteria, thereby eliminating competitors, analogous to quorum sensing for cooperative behavior such as social motility [20, 41, 43, 92]

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Summary

Introduction

Porphyromonas gingivalis is strongly implicated in the onset and progression of periodontitis, a chronic inflammatory disease of the gingival tissues with systemic impact on human health [1,2,3,4]. Due to its ability to orchestrate dysbiotic inflammation and disrupt host-microbial homeostasis even at low abundance, current

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