Control of bacterial virulence by membrane-less regulatory compartment

Escherichia coli is transformed from a commensal into a pathogen by acquisition of genetic elements called pathogenicity islands (PAIs). We investigated how the PAI virulence genes of enteropathogenic E. coli (EPEC) respond when the bacterium attaches to a host gut cell. EPEC first sticks to the host by means of pili and then employ a nano-syringe termed type 3 secretion system (T3SS) to inject multiple proteins termed effectors into the host cell. We show that the T3SS also functions to sense the host cell and to trigger in response a global posttranscriptional reprogramming of expression of virulence and metabolic genes. This regulation is mediated by an intricate network that includes RNA binding protein termed CsrA, several anti-CsrA factors and anti-anti-CsrA factors, all organize within the bacteria in a distinct cytoplasmic "organelle". This organelle seems to be widespread in pathogenic and nonpathogenic gram-negative bacteria. In the case of EPEC this regulation helps the bacteria to adapt to epithelial cell–associated lifestyle.