| Popis: |
Hfq (host factor for phage Q beta) is key for posttranscriptional generegulation in many bacteria. Hfq’s function is to stabilize sRNAs andto facilitate base-pairing withtrans-encoded target mRNAs. Lossof Hfq typically results in pleiotropic phenotypes, and, in the majorhuman pathogenVibrio cholerae, Hfq inactivation has been linkedto reduced virulence, failure to produce biofilms, and impaired in-tercellular communication. However, the RNA ligands of Hfq inV. choleraeare currently unknown. Here, we used RIP-seq (RNA immu-noprecipitation followed by high-throughput sequencing) analysis toidentify Hfq-bound RNAs inV. cholerae. Our work revealed 603 cod-ing and 85 noncoding transcripts associated with Hfq, including 44sRNAs originating from the 3′end of mRNAs. Detailed investigationof one of these latter transcripts, named FarS (fatty acid regulated sRNA),showed that this sRNA is produced by RNase E-mediated maturationof thefabB3′UTR, and, together with Hfq, inhibits the expression oftwo paralogousfadEmRNAs. ThefabBandfadEgenes are antag-onistically regulated by the major fatty acid transcription factor,FadR, and we show that, together, FadR, FarS, and FadE constitutea mixed feed-forward loop regulating the transition between fattyacid biosynthesis and degradation inV. cholerae. Our results providethe molecular basis for studies on Hfq inV. choleraeand highlight theimportance of a previously unrecognized sRNA for fatty acid metabo-lism in this major human pathogen. |
