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dc.contributor.authorCabot, Gabrieles_ES
dc.contributor.authorZamorano, Lauraes_ES
dc.contributor.authorMoyà, Bartolomées_ES
dc.contributor.authorJuan, Carloses_ES
dc.contributor.authorNavas, Alfonsoes_ES
dc.contributor.authorBlázquez Gómez, Jesúses_ES
dc.contributor.authorOliver, Antonioes_ES
dc.date.accessioned2019-05-29T12:40:15Z-
dc.date.available2019-05-29T12:40:15Z-
dc.date.issued2016-03-
dc.identifier.citationAntimicrobial Agents and Chemotherapy 60(3): 1767-1778 (2016)es_ES
dc.identifier.issn0066-4804-
dc.identifier.urihttp://hdl.handle.net/10261/182788-
dc.description.abstractPseudomonas aeruginosa, a major cause of nosocomial and chronic infections, is considered a paradigm of antimicrobial resistance development. However, the evolutionary trajectories of antimicrobial resistance and the impact of mutator phenotypes remain mostly unexplored. Therefore, whole-genome sequencing (WGS) was performed in lineages of wild-type and mutator (ΔmutS) strains exposed to increasing concentrations of relevant antipseudomonal agents. WGS provided a privileged perspective of the dramatic effect of mutator phenotypes on the accumulation of random mutations, most of which were transitions, as expected. Moreover, a frameshift mutagenic signature, consistent with error-prone DNA polymerase activity as a consequence of SOS system induction, was also seen. This effect was evidenced for all antibiotics tested, but it was higher for fluoroquinolones than for cephalosporins or carbapenems. Analysis of genotype versus phenotype confirmed expected resistance evolution trajectories but also revealed new pathways. Classical mechanisms included multiple mutations leading to AmpC overexpression (ceftazidime), quinolone resistance-determining region (QRDR) mutations (ciprofloxacin), oprD inactivation (meropenem), and efflux pump overexpression (ciprofloxacin and meropenem). Groundbreaking findings included gain-of-function mutations leading to the structural modification of AmpC (ceftazidime), novel DNA gyrase (GyrA) modification (ciprofloxacin), and the alteration of the β-lactam binding site of penicillin-binding protein 3 (PBP3) (meropenem). A further striking finding was seen in the evolution of meropenem resistance, selecting for specific extremely large (>250 kb) genomic deletions providing a growth advantage in the presence of the antibiotic. Finally, fitness and virulence varied within and across evolved antibiotic-resistant populations, but mutator lineages showed a lower biological cost for some antibiotics.es_ES
dc.language.isoenges_ES
dc.publisherAmerican Society for Microbiologyes_ES
dc.rightsclosedAccesses_ES
dc.titleEvolution of Pseudomonas aeruginosa Antimicrobial Resistance and Fitness under Low and High Mutation Rateses_ES
dc.typeartículoes_ES
dc.identifier.doi10.1128/AAC.02676-15-
dc.description.peerreviewedPeer reviewedes_ES
dc.relation.publisherversionhttps://doi.org/10.1128/AAC.02676-15es_ES
dc.identifier.e-issn1098-6596-
dc.relation.csices_ES
oprm.item.hasRevisionno ko 0 false*
dc.identifier.pmid26729493-
dc.type.coarhttp://purl.org/coar/resource_type/c_6501es_ES
item.openairetypeartículo-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.grantfulltextnone-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
item.fulltextNo Fulltext-
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