Question

How does quorum sensing promote pathogenesis?  Why might this physiology have evolved?

What are the different regulatory circuits associated with quorum sensing and how do they compare/contrast for AIP vs. AHL autoinducers?

In the various presented quorum sensing systems, which proteins are involved in synthesizing and sensing the autoinducer. What kind of autoinducers (autoinducer peptide vs. AHLs) are associated with specific quorum sensing systems?

Answer 1

The phenomenon of quorum sensing, or cell-to-cell communication, relies on the principle that when a single bacterium releases autoinducers (AIs) into the environment, their concentration is too low to be detected.

Quorum sensing in gram-negative organisms involves two regulatory components: the transcriptional activator protein (R protein) and the AI molecule produced by the autoinducer synthase. Accumulation of AI occurs in a cell-density-dependent manner until a threshold level is reached. At this time the AI binds to and activates the R protein, which in turn induces gene expression. The R protein consists of two domains: the N terminus of the protein that interacts with AI and the C terminus that is involved in DNA binding. Typically, gram-negative AI molecules are N-acyl-HSLs; however, other types of signal molecules do exist.

The signal molecules, known as autoinducers, are secreted into the environment by bacteriaand gradually increase in concentration as thebacteria population grows. ... For example, thebacterium Pseudomonas aeruginosa, which can cause pneumonia and blood infections, uses quorum sensing to regulate diseasemechanisms.

A cognate LuxR-like protein is responsible for recognition of the AHL and when bound to the AHL, LuxR-like protein binds to specific promoter DNA elements and activates transcription of target genes (Figure 1). ... The LuxI/LuxR–type quorum sensing in Gram-negative bacteria.

Acylated homoserine lactones, peptide, are examples for autoinducers.