High on the list of the exciting manners bacteria communicate with one another is quorum sensing (QS), a population-dependent gene regulation system that operates within a wide range of species. The general scheme of QS is as follows: at high population densities, signal molecules called autoinducers reach threshold levels, at which point they initiate a signal transduction pathway leading to transcription of specific genes. This altered gene expression allows the bacterial community to behave in a cooperative manner so as to achieve a common goal. In a sense, the bacterial population now functions like a multicellular organism. In many Proteobacteria, such as vibrios and pseudomonads, autoinducers are acyl-homoserine lactones (AHLs), compounds synthesized by the LuxI family of signal synthases and detected by the LuxR family of transcriptional regulators. Cellular activities regulated by AHLs include bioluminescence, biofilm formation, motility, and the making of virulence factors, among others. A large body of studies has illuminated the molecular mechanisms underlying QS, but identifying what’s in it for the species has not always been easy. In the paper to be discussed here, Goo and collaborators show how QS enables bacteria to avoid the perils of entry into stationary phase.
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