Fig. 1

Representations of N-acyl homoserine lactone (AHL), autoinducer-2 (AI-2), and autoinducing peptide (AIP) mediated quorum sensing (QS). A Bacteria produce AHLs via the LuxI synthase, which are released into the extracellular environment. At low cell density, AHL concentrations outside the cell remain low, leading to inactive QS. B As bacterial density increases, the concentration of AHLs increases, causing entry into the cell. AHLs bind to their corresponding cytoplasmic LuxR receptors, which initiates the expression of target genes, including the production of additional AHLs. C Similarly, AI-2 is produced via the LuxS synthase and is released into the extracellular space. At low cell density, AI-2 does not activate gene expression. Pre-AIPs, which are encoded by agrD, leave the bacteria through AgrB, a membrane receptor. Without sufficient concentration, gene expression will not be activated. D Increased bacterial density leads to AI-2 entry into the cell, where it binds LuxP and LsrB receptors, which initiate the expression of target genes. As the concentration of extracellular AIPs increases, more binding with AgrC occurs, which initiates the phosphorylation of AgrA and subsequent activation of target genes. Figures created using BioRender