More than Just a Quorum: Integration of Stress and Other Environmental Cues in Acyl-Homoserine Lactone Signaling

Abstract

Many bacteria employ chemical communication to coordinate group behaviors, a process that has been termed quorum sensing (QS). Although many different classes of bacteria use QS, the mechanism that has emerged as common in gram-negative proteobacteria is based on acyl-homoserine lactone (acyl-HSL) signal molecules. QS is an important field of study because of its important regulatory roles in pathogenic and environmental bacteria. Acyl-homoserine lactone (Acyl-HSL) QS controls virulence in many plant and animal pathogens such as Pseudomonas aeruginosa, Burkholderia cepacia, and Agrobacterium tumefaciens. This chapter focuses on the integration of acyl-HSL QS and such stress responses. In P. aeruginosa, QS controls the expression of numerous virulence factors such as extracellular enzymes (LasB elastase, LasA protease, alkaline protease), secondary metabolites (pyocyanin, hydrogen cyanide, pyoverdin), and toxins (exotoxin A). Microarray studies revealed that the las and rhl systems together control the expression of more than 300 genes. The majority of the associated genes are predicted to encode secreted factors and secretion machinery, confirming the notion that the core function of las QS is to control the expression of extracellular factors. Indeed, a recent population analysis of concurrently isolated P. aeruginosa from individual Cystic fibrosis (CF) lung infections revealed great heterogeneity of QS phenotypes and genotypes within as well as among patients. This finding suggests that a single selective mechanism, whether of social or nonsocial nature, is unlikely to explain the emergence of QS variants during CF infection.