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Novel targets of the CbrAB/Crc carbon catabolite control system revealed by transcript abundance in Pseudomonas aeruginosa.

Détails de la publication Détails dans Serval
ID Serval serval:BIB_C4DE67653221
Type de publication
Article: article d'un périodique ou d'un magazine.
Collection Publications
Fonds UNIL/CHUV
Auteur(s) Sonnleitner E., Valentini M., Wenner N., Haichar Fel Z, Haas D., Lapouge K.
Titre Novel targets of the CbrAB/Crc carbon catabolite control system revealed by transcript abundance in Pseudomonas aeruginosa.
Périodique PLoS One
Statut éditorial Publié
Année 2012
Peer-reviewed oui
Volume 7
Numéro 10
Pages e44637
Langue anglais
Résumé The opportunistic human pathogen Pseudomonas aeruginosa is able to utilize a wide range of carbon and nitrogen compounds, allowing it to grow in vastly different environments. The uptake and catabolism of growth substrates are organized hierarchically by a mechanism termed catabolite repression control (Crc) whereby the Crc protein establishes translational repression of target mRNAs at CA (catabolite activity) motifs present in target mRNAs near ribosome binding sites. Poor carbon sources lead to activation of the CbrAB two-component system, which induces transcription of the small RNA (sRNA) CrcZ. This sRNA relieves Crc-mediated repression of target mRNAs. In this study, we have identified novel targets of the CbrAB/Crc system in P. aeruginosa using transcriptome analysis in combination with a search for CA motifs. We characterized four target genes involved in the uptake and utilization of less preferred carbon sources: estA (secreted esterase), acsA (acetyl-CoA synthetase), bkdR (regulator of branched-chain amino acid catabolism) and aroP2 (aromatic amino acid uptake protein). Evidence for regulation by CbrAB, CrcZ and Crc was obtained in vivo using appropriate reporter fusions, in which mutation of the CA motif resulted in loss of catabolite repression. CbrB and CrcZ were important for growth of P. aeruginosa in cystic fibrosis (CF) sputum medium, suggesting that the CbrAB/Crc system may act as an important regulator during chronic infection of the CF lung.
ISBN/ISSN 1932-6203 (Electronic)
ISSN-L 1932-6203
URN urn:nbn:ch:serval-BIB_C4DE676532216
OAI oai:serval.unil.ch:BIB_C4DE67653221
DOI 10.1371/journal.pone.0044637
Référence externe Pubmed : 23115619
Référence externe Web of Science : 000310310200006
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Dernière modification 2013-03-11

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