Format

Send to

Choose Destination
PLoS Genet. 2014 Jun 19;10(6):e1004440. doi: 10.1371/journal.pgen.1004440. eCollection 2014 Jun.

Regulation of Hfq by the RNA CrcZ in Pseudomonas aeruginosa carbon catabolite repression.

Author information

1
Department of Microbiology, Immunobiology and Genetics, Max F. Perutz Laboratories, Center of Molecular Biology, University of Vienna, Vienna, Austria.

Abstract

Carbon Catabolite repression (CCR) allows a fast adaptation of Bacteria to changing nutrient supplies. The Pseudomonas aeruginosa (PAO1) catabolite repression control protein (Crc) was deemed to act as a translational regulator, repressing functions involved in uptake and utilization of carbon sources. However, Crc of PAO1 was recently shown to be devoid of RNA binding activity. In this study the RNA chaperone Hfq was identified as the principle post-transcriptional regulator of CCR in PAO1. Hfq is shown to bind to A-rich sequences within the ribosome binding site of the model mRNA amiE, and to repress translation in vitro and in vivo. We further report that Crc plays an unknown ancillary role, as full-fledged repression of amiE and other CCR-regulated mRNAs in vivo required its presence. Moreover, we show that the regulatory RNA CrcZ, transcription of which is augmented when CCR is alleviated, binds to Hfq with high affinity. This study on CCR in PAO1 revealed a novel concept for Hfq function, wherein the regulatory RNA CrcZ acts as a decoy to abrogate Hfq-mediated translational repression of catabolic genes and thus highlights the central role of RNA based regulation in CCR of PAO1.

PMID:
24945892
PMCID:
PMC4063720
DOI:
10.1371/journal.pgen.1004440
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Public Library of Science Icon for PubMed Central
Loading ...
Support Center