In biology, quorum sensing or quorum signaling (QS) is the process of cell-to-cell communication that allows bacteria to detect and respond to cell population density by gene regulation, typically as a means of acclimating to environmental disadvantages. Quorum sensing is a type of cellular signaling, and can be more specifically considered a type of paracrine signaling. However, it also contains traits of autocrine signaling: a cell produces both an autoinducer molecule and the receptor for the autoinducer. As one example, quorum sensing enables bacteria to restrict the expression of specific genes to the high cell densities at which the resulting phenotypes will be most beneficial, especially for phenotypes that would be ineffective at low cell densities and therefore too energetically costly to express. Many species of bacteria use quorum sensing to coordinate gene expression according to the density of their local population. In a similar fashion, some social insects use quorum sensing to determine where to nest. Quorum sensing in pathogenic bacteria activates host immune signaling and prolongs host survival, by limiting the bacterial intake of nutrients, such as tryptophan, which further is converted to serotonin. As such, quorum sensing allows a commensal interaction between host and pathogenic bacteria. Quorum sensing may also be useful for cancer cell communications. In addition to its function in biological systems, quorum sensing has several useful applications for computing and robotics. In general, quorum sensing can function as a decision-making process in any decentralized system in which the components have: (a) a means of assessing the number of other components they interact with and (b) a standard response once a threshold of the number of components is detected.
Discovery The first observations of an autoinducer-controlled phenotype in bacteria were reported in 1970, by Kenneth Nealson, Terry Platt, and J. Woodland Hastings, who observed what they described as a conditioning of the medium in which they had grown the bioluminescent marine bacterium Aliivibrio fischeri. These bacteria did not synthesize luciferase—and therefore did not luminesce—in freshly inoculated culture but only after the bacterial population had increased significantly. In a series of publications from 1998 to 2001, Bonnie Bassler showed that quorum sensing is not just an isolated mechanism in Aliivibrio fischeri, but is used ubiquitously across bacteria to communicate. This advance demonstrated that bacteria are capable of carrying out complex, collective behaviors.
Etymology Because Nealson, Platt, and Hastings attributed the conditioning of the growth medium to the growing population of cells itself, they referred to the phenomenon as autoinduction. In 1994, after study of the phenomenon had expanded into several additional bacteria, Stephen Winans did not believe the word autoinduction fully characterized the true process so, in a review article coauthored with W. Claiborne Fuqua and E. Peter Greenberg, he introduced the term quorum sensing. Its use also avoided confusion between the terms autoinduction and autoregulation. The new term was not stumbled onto, but rather created through trial and error. Among the alternatives that Winans had created and considered were gridlockins, communiolins, and quoromones.
Bacteria
Some of the best-known examples of quorum sensing come from studies of bacteria. Bacteria use quorum sensing to regulate certain phenotype expressions, which in turn, coordinate their behaviors. Some common phenotypes include biofilm formation, virulence factor expression, and motility. Certain bacteria are able to use quorum sensing to regulate bioluminescence, nitrogen fixation and sporulation. The quorum-sensing function is based on the local density of the bacterial population in the immediate environment. It can occur within a single bacterial species, as well as between diverse species. Both gram-positive and gram-negative bacteria use quorum sensing, but there are some major differences in their mechanisms.
Mechanism For the bacteria to use quorum sensing constitutively, they must possess three abilities: secretion of a signaling molecule, secretion of an autoinducer (to detect the change in concentration of signaling molecules), and regulation of gene transcription as a response. This process is highly dependent on the diffusion mechanism of the signaling molecules. QS signaling molecules are usually secreted at a low level by individual bacteria. At low cell density, the molecules may just diffuse away. At high cell density, the local concentration of signaling molecules may exceed its threshold level, and trigger changes in gene expression.
Gram-positive bacteria Gram-positive bacteria use autoinducing peptides (AIP) as their autoinducers. When gram-positive bacteria detect high concentration of AIPs in their environment, that happens by way of AIPs binding to a receptor to activate a kinase. The kinase phosphorylates a transcription factor, which regulates gene transcription. This is called a two-component system. Another possible mechanism is that AIP is transported into the cytosol, and binds directly to a transcription factor to initiate or inhibit transcription.
Gram-negative bacteria Gram-negative bacteria produce N-acyl homoserine lactones (AHL) as their signaling molecule. Usually AHLs do not need additional processing, and bind directly to transcription factors to regulate gene expression. Some gram-negative bacteria may use two-component systems as well.
Examples
Aliivibrio fischeri The bioluminescent bacterium Aliivibrio fischeri is the first organism in which QS was observed. It lives as a mutualistic symbiont in the photophore (or light-producing organ) of the Hawaiian bobtail squid. When A. fischeri cells are free-living (or planktonic), the autoinducer is at low concentration, and, thus, cells do not show luminescence. However, when the population reaches the threshold in the photophore (about 1011 cells/ml), transcription of luciferase is induced, leading to bioluminescence. In A. fischeri, bioluminescence is regulated by AHLs (N-acyl-homoserine lactones) which is a product of the LuxI gene whose transcription is regulated by the LuxR activator. LuxR works only when AHLs binds to the LuxR.
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