Bacteria use chemical signals called autoinducers to communicate with one another — a phenomenon known as quorum sensing. By producing and importing autoinducers, bacterial cells establish the density of their own and other species and synchronize the expression of fundamental genes. Now, a new report published in Nature shows that certain bacteria can interfere with autoinducer-mediated signals, disrupting quorum-sensing behaviour in competing microorganisms.

Previous work by Karina Xavier and Bonnie Bassler had characterized the quorum-sensing mechanisms of Escherichia coli and Vibrio harveyi: both species communicate using the autoinducer AI-2. A positive feedback loop operates in E. coli — consumption of AI-2 induces the expression of the lsr operon, which encodes the transporter that imports AI-2. In V. harveyi, detection of AI-2 by extracytoplasmic receptors modulates the expression of genes that are involved in bioluminescence and type three secretion.

In this study, the authors first confirmed that E. coli and V. harveyi communicated using AI-2. Co-culture experiments showed that AI-2 production by either E. coli or V. harveyi induced the expression of the E. coli lsr operon. Similarly, in V. harveyi, AI-2 from either species activated the bioluminescence genes and repressed type-three-secretion genes. This cross-species communication is especially interesting as E. coli and V. harveyi detect AI-2 signals with different chemical structures, and chemical interconversion presumably takes place in the surrounding media.

In mixed consortia, the induction of quorum-sensing genes by AI-2 is not equivalent in different species. In model V. harveyi–E. coli cultures, the consumption of AI-2 by E. coli interfered with the expression of the V. harveyi quorum-sensing regulon, reducing light production and de-repressing a type-three-secretion locus.

Furthermore, E. coli AI-2 consumption interfered with the quorum-sensing behaviour of Vibrio cholerae , extending these observations to communities that could co-colonize the human enteric system.

The authors conclude with an intriguing proposal — perhaps eukaryotes have developed specific associations with microorganisms that communicate using AI-2. The manipulation of AI-2 signals by these bacteria would maintain normal eukaryotic microflora and protect the host against pathogenic bacteria.