Date Published: July 7, 2017
Publisher: Public Library of Science
Author(s): Elisabeth Sonnleitner, Konstantin Prindl, Udo Bläsi, Lennart Randau.
The RNA chaperone Hfq regulates virulence and metabolism in the opportunistic pathogen Pseudomonas aeruginosa. During carbon catabolite repression (CCR) Hfq together with the catabolite repression control protein Crc can act as a translational repressor of catabolic genes. Upon relief of CCR, the level of the Hfq-titrating RNA CrcZ is increasing, which in turn abrogates Hfq-mediated translational repression. As the interdependence of Hfq-mediated and RNA based control mechanisms is poorly understood, we explored the possibility whether the regulatory RNA CrcZ can interfere with riboregulation. We first substantiate that the P. aeruginosa Hfq is proficient and required for riboregulation of the transcriptional activator gene antR by the small RNA PrrF1-2. Our studies further revealed that CrcZ can interfere with PrrF1-2/Hfq-mediated regulation of antR. The competition for Hfq can be rationalized by the higher affinity of Hfq for CrcZ than for antR mRNA.
Numerous studies have been performed during the last decade to decipher the function and structure of the RNA chaperone Hfq. Most studies were conducted in E. coli, and it is now well established that Hfq fulfills several functions in post-transcriptional regulation. It can stabilize small regulatory RNAs (sRNAs) and facilitate annealing between sRNAs and their target mRNAs. The latter mode of action may result either in translational repression accompanied by degradation of both RNAs or in translational activation and stabilization of the mRNA. In addition, it may stimulate polyadenylation of mRNAs, which can trigger 3´ to 5´directional decay . Moreover, there is accumulating evidence that Hfq can act per se as a translational repressor of mRNAs [2–4].