The name quorum sensing (QS) was then coined

The name quorum sensing (QS) was then coined selleck chem Z-VAD-FMK in the 1990s [4] to denote this cell-cell communication mechanism which is now recognized as a key trait governing bacterial community behavior [5�C7]. In this mechanism, chemical signals trigger cellular Inhibitors,Modulators,Libraries 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 Inhibitors,Modulators,Libraries 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]. Luxl-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 Inhibitors,Modulators,Libraries 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 Inhibitors,Modulators,Libraries 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 QS Cilengitide signaling molecules discovered so far; as of today over 70 species have been reported to possess N-AHL all targets QS systems (see [17] for an earlier review).

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