What doesn't kill you...

Vibrio cholerae is a species of bacteria that causes cholera by producing a toxin that disrupts the intestinal lining, leading to severe diarrhea, dehydration, and potentially death if left untreated. The Molecular Microbiology Group (Marc Erhardt) investigated the role of the RNA chaperone ProQ in post-transcriptional gene regulation within Vibrio cholerae. Employing RIL-Seq, they identified a vast network of ProQ-assisted RNA interactions, revealing a crucial role for the FlaX sRNA in regulating bacterial motility, which contributes decisively to the pathogenicity of the bacterium. If you want to obtain a comprehensive view of ProQ-mediated RNA regulation and its impact on bacterial virulence in V. cholerae, check out their Nucleic Acids Research Article!

Abstract

Gene regulation at the post-transcriptional level is prevalent in all domains of life. In bacteria, ProQ-like proteins have emerged as important RNA chaperones facilitating RNA stability and RNA duplex formation. In the major human pathogen Vibrio cholerae, post-transcriptional gene regulation is key for virulence, biofilm formation, and antibiotic resistance, yet the role of ProQ has not been studied. Here, we show that ProQ interacts with hundreds of transcripts in V. cholerae, including the highly abundant FlaX small RNA (sRNA). Global analyses of RNA duplex formation using RIL-Seq (RNA interaction by ligation and sequencing) revealed a vast network of ProQ-assisted interactions and identified a role for FlaX in motility regulation. Specifically, FlaX base-pairs with multiple sites on the flaB flagellin mRNA, preventing 30S ribosome binding and translation initiation. V. cholerae cells lacking flaX display impaired motility gene expression, altered flagella composition and reduced swimming in liquid environments. Our results provide a global view on ProQ-associated RNA duplex formation and pinpoint the mechanistic and phenotypic consequences associated with ProQ-associated sRNAs in V. cholerae.