Summary
Bacterial pathogens employ a plethora of virulence factors for host invasion, and their use is tightly regulated to maximize infection efficiency and manage resources in a nutrient-limited environment. Here we show that during Escherichia coli stationary phase the small non-coding RNA fimR2 regulates fimbrial and flagellar biosynthesis at the post-transcriptional level, leading to biofilm formation as the dominant mode of survival under conditions of nutrient depletion. fimR2 interacts with the translational regulator CsrA, antagonizing its functions and firmly tightening control over motility and biofilm formation. Generated through RNase E cleavage, fimR2 regulates stationary phase biology independently of the chaperones Hfq and ProQ. The Salmonella enterica version of fimR2 induces effector protein secretion by the type III secretion system and stimulates infection, thus linking the sRNA to virulence. This work reveals the importance of bacterial sRNAs in modulating various aspects of bacterial physiology including stationary phase and virulence.
Highlights
fimR2 expression causes biofilm formation and alters bacterial outer membrane architecture
fimR2 modulates CsrA activity and sequesters it from its targets
The Salmonella fimR2 variant is functional in E. coli
fimR2 is generated through RNase E processing and enhances infectivity
Competing Interest Statement
The authors have declared no competing interest.
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