<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>5(1)</volume><submitter>Tahrioui A</submitter><pubmed_abstract>Biofilms are structured microbial communities that are the leading cause of numerous chronic infections which are difficult to eradicate. Within the lungs of individuals with cystic fibrosis (CF), &lt;i>Pseudomonas aeruginosa&lt;/i> causes persistent biofilm infection that is commonly treated with aminoglycoside antibiotics such as tobramycin. However, sublethal concentrations of this aminoglycoside were previously shown to increase biofilm formation by &lt;i>P. aeruginosa&lt;/i>, but the underlying adaptive mechanisms still remain elusive. Herein, we combined confocal laser scanning microscope analyses, proteomics profiling, gene expression assays and phenotypic studies to unravel &lt;i>P. aeruginosa&lt;/i> potential adaptive mechanisms in response to tobramycin exposure during biofilm growth. Under this c</pubmed_abstract><journal>NPJ biofilms and microbiomes</journal><pagination>15</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC6533273</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Extracellular DNA release, quorum sensing, and PrrF1/F2 small RNAs are key players in &lt;i>Pseudomonas aeruginosa&lt;/i> tobramycin-enhanced biofilm formation.</pubmed_title><pmcid>PMC6533273</pmcid><pubmed_authors>Rodrigues S</pubmed_authors><pubmed_authors>Bouffartigues E</pubmed_authors><pubmed_authors>Groleau MC</pubmed_authors><pubmed_authors>Lesouhaitier O</pubmed_authors><pubmed_authors>Brenner-Weiss G</pubmed_authors><pubmed_authors>Feuilloley M</pubmed_authors><pubmed_authors>Duchesne R</pubmed_authors><pubmed_authors>Tortuel D</pubmed_authors><pubmed_authors>Maillot O</pubmed_authors><pubmed_authors>Dufour A</pubmed_authors><pubmed_authors>Chevalier S</pubmed_authors><pubmed_authors>Tahrioui A</pubmed_authors><pubmed_authors>Hardouin J</pubmed_authors><pubmed_authors>Deziel E</pubmed_authors><pubmed_authors>Taupin L</pubmed_authors><pubmed_authors>Orange N</pubmed_authors><pubmed_authors>Cornelis P</pubmed_authors></additional><is_claimable>false</is_claimable><name>Extracellular DNA release, quorum sensing, and PrrF1/F2 small RNAs are key players in &lt;i>Pseudomonas aeruginosa&lt;/i> tobramycin-enhanced biofilm formation.</name><description>Biofilms are structured microbial communities that are the leading cause of numerous chronic infections which are difficult to eradicate. Within the lungs of individuals with cystic fibrosis (CF), &lt;i>Pseudomonas aeruginosa&lt;/i> causes persistent biofilm infection that is commonly treated with aminoglycoside antibiotics such as tobramycin. However, sublethal concentrations of this aminoglycoside were previously shown to increase biofilm formation by &lt;i>P. aeruginosa&lt;/i>, but the underlying adaptive mechanisms still remain elusive. Herein, we combined confocal laser scanning microscope analyses, proteomics profiling, gene expression assays and phenotypic studies to unravel &lt;i>P. aeruginosa&lt;/i> potential adaptive mechanisms in response to tobramycin exposure during biofilm growth. Under this c</description><dates><release>2019-01-01T00:00:00Z</release><publication>2019</publication><modification>2025-04-04T21:40:24.554Z</modification><creation>2019-07-01T13:54:51Z</creation></dates><accession>S-EPMC6533273</accession><cross_references><pubmed>31149345</pubmed><doi>10.1038/s41522-019-0088-3</doi></cross_references></HashMap>