Cell–cell signalling in bacteria: not simply a matter of quorum

Abstract

Bacterial signalling known as quorum sensing (QS) relies on the synthesis of autoinducing signals throughout growth; when a threshold concentration is reached, these signals interact with a transcriptional regulator, allowing the expression of specific genes at a high cell density. One of the most studied intraspecies signalling is based on the use of N-acyl-homoserine lactones (AHL). Many factors other than cell density were shown to affect AHL accumulation and interfere with the QS signalling process. At the cellular level, the genetic determinants of QS are integrated in a complex regulatory network, including QS cascades and various transcriptional and post-transcriptional regulators that affect the synthesis of the AHL signal. In complex environments where bacteria exist, AHL do not accumulate at a constant rate; the diffusion and perception of the AHL signal outside bacterial cells can be compromised by abiotic environmental factors, by members of the bacterial community such as AHL-degrading bacteria and also by compounds produced by eukaryotes acting as an AHL mimic or inhibitor. This review aims to present all factors interfering with the AHL-mediated signalling process, at the levels of signal production, diffusion and perception.