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

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 sourc...

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Published in:PLoS genetics 2014-06, Vol.10 (6), p.e1004440-e1004440
Main Authors: Sonnleitner, Elisabeth, Bläsi, Udo
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description 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.
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fellowships</topic><topic>Signal transduction</topic><topic>Standard deviation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sonnleitner, Elisabeth</creatorcontrib><creatorcontrib>Bläsi, Udo</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints database</collection><collection>Gale In Context: Canada</collection><collection>Gale In Context: Science</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>Directory of Open Access Journals</collection><jtitle>PLoS genetics</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sonnleitner, Elisabeth</au><au>Bläsi, Udo</au><au>Garsin, Danielle A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Regulation of Hfq by the RNA CrcZ in Pseudomonas aeruginosa carbon catabolite repression</atitle><jtitle>PLoS genetics</jtitle><addtitle>PLoS Genet</addtitle><date>2014-06-01</date><risdate>2014</risdate><volume>10</volume><issue>6</issue><spage>e1004440</spage><epage>e1004440</epage><pages>e1004440-e1004440</pages><issn>1553-7404</issn><issn>1553-7390</issn><eissn>1553-7404</eissn><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.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24945892</pmid><doi>10.1371/journal.pgen.1004440</doi><oa>free_for_read</oa></addata></record>
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subjects Amidohydrolases - antagonists & inhibitors
Amidohydrolases - genetics
Amidohydrolases - metabolism
Analysis
Bacteria
Bacteriology
Binding sites
Biology and Life Sciences
Carbon
Carbon - metabolism
Catabolite Repression - genetics
Experiments
Gene Expression Regulation, Bacterial
Genetic aspects
Genetic regulation
Host Factor 1 Protein - genetics
Physiological aspects
Proteins
Pseudomonas aeruginosa
Pseudomonas aeruginosa - genetics
Pseudomonas aeruginosa - metabolism
Pseudomonas Infections
Regulation
Regulatory Sequences, Ribonucleic Acid - genetics
Ribosomes - metabolism
RNA
RNA Processing, Post-Transcriptional
RNA, Bacterial - genetics
RNA, Messenger - genetics
RNA-Binding Proteins - genetics
Scholarships & fellowships
Signal transduction
Standard deviation
title Regulation of Hfq by the RNA CrcZ in Pseudomonas aeruginosa carbon catabolite repression
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