## 1 Introduction  
Bacteria might be simple, single celled organisms but their social behavior means they can form complex communities and engage in coordinated behaviors. Many bacterial species use chemical signals to monitor their environment and regulate population density. A pioneering study in bacterial chemical signaling was the unraveling of the regulation of luminescence in the marine bacterium _Vibrio fischeri_ through a self-produced signal termed autoinducer [1]. _V. fischeri_ regulates light production in the Hawaiian bobtail squid (_Euprymna scolopes_); when the population of _V. fischeri_ reaches a certain density in the light organ of the squid, the concentration of the signaling molecule, exceeds a threshold extra-cellularly, triggering a cascade of cellular events that finally manifest in the production of light. More than 10 years later the signal was identified as an acyl homoserine lactone (AHL; [2]) and the genetic circuit was then also identified and shown to be composed of a signal generator called the _luxI_/LuxI gene/protein and a response-regulatory protein designated as _luxR_/LuxR gene/protein [3]. The name quorum sensing (QS) was then coined in the 1990s [4] to denote this cell-cell communication mechanism which is now recognized as a key trait governing bacterial community behavior [5; 6; 7]. In this mechanism, chemical signals trigger cellular actions such as cell division, the production of virulence factors as well as other traits that aid survival. Cross-talk between bacterial species may also determine survival in complex microbiota. Even inter-kingdom communication routes have been identified, including bacterial-fungal and plant-bacterium interactions [8; 9]. The importance of quorum sensing has been clear for a number of years as it appears to be a promising target for controlling bacterial colonization and pathogenesis in human disease [10]. This could be of particular importance, as multidrug resistant strains of human pathogens continue to emerge. Potentially beneficial effects in relation to plant health can be attributed to QS in certain species including regulation of the production of anti-microbial compounds and induction of systemic resistance in plants [11]. One of the most well studied cellular and genetic mechanisms of QS is based on the \(N\)-acylhomoserine lactones (N-AHLs) [4]. Bacterial cells secrete and respond to autoinducers continuously to sense the surrounding environment, and respond to events as they occur. When an autoinducer reaches a critical level, the population of bacteria responds through a coordinated expression of specific target genes, which finally manifest in a particular behavior/phenotype. The N-AHL QS system is based on two proteins belonging to the LuxI and LuxR families [5; 12]. LuxI-family proteins are cytoplasmic enzymes and are responsible for N-AHL synthesis [13]. After synthesis, the signal molecule moves freely across cell membranes and accumulates both intra- and extra-cellularly in proportion to cell density. When populations are low, N-AHL dissipates; when populations are high, N-AHL concentration increases. Above a critical concentration or cell density, N-AHLs interact with the LuxR-family [14] which in most cases result in complexes (homodimers) that bind specific promoter DNA sequences (termed _lux_-boxes) located in the promoter region of target QS-regulated genes ([15]. This subsequently affects their expression resulting in particular phenotypes of the organism. Most often one of the targets of AHL QS is the _luxI_-family gene resulting in a positive feedback loop. As sequencing technologies have improved and many more bacterial genomes have been sequenced, it has become apparent that homologues of key _V. fischeri_ N-AHL QS genes are present in the genomes of many Gram-negative bacteria [16; 17]. N-AHLs are one of the most studied QSsignaling molecules discovered so far; as of today over 70 species have been reported to possess N-AHL QS systems (see [17] for an earlier review).