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      The small RNA chaperone Hfq and multiple small RNAs control quorum sensing in Vibrio harveyi and Vibrio cholerae.

      Cell
      Amino Acid Sequence, Computational Biology, Conserved Sequence, Gene Deletion, Gene Expression Regulation, Bacterial, Genes, Bacterial, Genes, Regulator, Host Factor 1 Protein, genetics, metabolism, Luciferases, Luminescent Measurements, MicroRNAs, chemistry, Models, Biological, Molecular Sequence Data, Mutagenesis, Insertional, Protein Structure, Secondary, RNA, Messenger, Repressor Proteins, Sequence Homology, Amino Acid, Signal Transduction, Vibrio, physiology, Vibrio cholerae, pathogenicity, Virulence

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          Abstract

          Quorum-sensing bacteria communicate with extracellular signal molecules called autoinducers. This process allows community-wide synchronization of gene expression. A screen for additional components of the Vibrio harveyi and Vibrio cholerae quorum-sensing circuits revealed the protein Hfq. Hfq mediates interactions between small, regulatory RNAs (sRNAs) and specific messenger RNA (mRNA) targets. These interactions typically alter the stability of the target transcripts. We show that Hfq mediates the destabilization of the mRNA encoding the quorum-sensing master regulators LuxR (V. harveyi) and HapR (V. cholerae), implicating an sRNA in the circuit. Using a bioinformatics approach to identify putative sRNAs, we identified four candidate sRNAs in V. cholerae. The simultaneous deletion of all four sRNAs is required to stabilize hapR mRNA. We propose that Hfq, together with these sRNAs, creates an ultrasensitive regulatory switch that controls the critical transition into the high cell density, quorum-sensing mode.

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