Quorum sensing controls Vibrio cholerae multicellular aggregate formation.

Matthew Jemielita,Ned S Wingreen,Bonnie L Bassler

doi:10.7554/elife.42057

Abstract

Bacteria communicate and collectively regulate gene expression using a process called quorum sensing (QS). QS relies on group-wide responses to signal molecules called autoinducers. Here, we show that QS activates a new program of multicellularity in Vibrio cholerae. This program, which we term aggregation, is distinct from the canonical surface-biofilm formation program, which QS represses. Aggregation is induced by autoinducers, occurs rapidly in cell suspensions, and does not require cell division, features strikingly dissimilar from those characteristic of V. cholerae biofilm formation. Extracellular DNA limits aggregate size, but is not sufficient to drive aggregation. A mutagenesis screen identifies genes required for aggregate formation, revealing proteins involved in V. cholerae intestinal colonization, stress response, and a protein that distinguishes the current V. cholerae pandemic strain from earlier pandemic strains. We suggest that QS-controlled aggregate formation is important for V. cholerae to successfully transit between the marine niche and the human host.

Highlights

Quorum sensing (QS) is a cell–cell communication process that bacteria use to orchestrate collective behaviors
V. cholerae cells carrying luxO D61E and luxO D61A are locked in the low cell density (LCD) and high cell density (HCD) QS-states, respectively
Aggregate formation occurs when V. cholerae cells are in a HCD QS-state, a QS-regulation pattern opposite to that for surface-biofilm formation which occurs when cells are in a LCD QS-state (Hammer and Bassler, 2003; Zhu and Mekalanos, 2003)

Summary

Introduction

Quorum sensing (QS) is a cell–cell communication process that bacteria use to orchestrate collective behaviors. At low cell density (LCD), when autoinducer concentration is low, QS promotes gene expression programs that benefit individual bacteria. At high cell density (HCD), when autoinducer concentration exceeds the threshold required for detection, QS drives gene expression programs beneficial to the community. Qrr activate translation of AphA and repress translation of HapR; respectively the master LCD and master HCD QS regulators (Lenz et al, 2004; Rutherford et al, 2011). At LCD, AphA is made and HapR is not, and V. cholerae cells act as individuals (Figure 1A). When bound to their cognate autoinducers, which occurs at HCD, CqsS and LuxPQ switch from acting as kinases to acting as phosphatases, dephosphorylating LuxO, via LuxU.

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