Cyclic AMP regulates bacterial persistence through repression of the oxidative stress response and SOS-dependent DNA repair in uropathogenic Escherichia coli

Vista sencilla de ítem
dc.contributor.authorMolina-Quiroz, Roberto C.
dc.contributor.authorSilva-Valenzuela, Cecilia
dc.contributor.authorBrewster, Jennifer
dc.contributor.authorCastro-Nallar, Eduardo
dc.contributor.authorLevy, Stuart B.
dc.contributor.authorCamilli, Andrew
dc.date.accessioned2022-10-12T22:40:31Z
dc.date.available2022-10-12T22:40:31Z
dc.date.issued2018-01
dc.descriptionIndexación Scopuses
dc.description.abstractBacterial persistence is a transient, nonheritable physiological state that provides tolerance to bactericidal antibiotics. The stringent response, toxin-antitoxin modules, and stochastic processes, among other mechanisms, play roles in this phenomenon. How persistence is regulated is relatively ill defined. Here we show that cyclic AMP, a global regulator of carbon catabolism and other core processes, is a negative regulator of bacterial persistence in uropathogenic Escherichia coli, as measured by survival after exposure to a β-lactam antibiotic. This phenotype is regulated by a set of genes leading to an oxidative stress response and SOS-dependent DNA repair. Thus, persister cells tolerant to cell wall-acting antibiotics must cope with oxidative stress and DNA damage and these processes are regulated by cyclic AMP in uropathogenic E. coli. IMPORTANCE Bacterial persister cells are important in relapsing infections in patients treated with antibiotics and also in the emergence of antibiotic resistance. Our results show that in uropathogenic E. coli, the second messenger cyclic AMP negatively regulates persister cell formation, since in its absence much more persister cells form that are tolerant to β-lactams antibiotics. We reveal the mechanism to be decreased levels of reactive oxygen species, specifically hydroxyl radicals, and SOS-dependent DNA repair. Our findings suggest that the oxidative stress response and DNA repair are relevant pathways to target in the design of persister-specific antibiotic compounds. © 2018 Molina-Quiroz et al.es
dc.description.urihttps://journals-asm-org.recursosbiblioteca.unab.cl/doi/10.1128/mBio.02144-17
dc.identifier.citationmBio Volume 9, Issue 1 January-February 2018 Article number e02144-17es
dc.identifier.doi10.1128/mBio.02144-17
dc.identifier.issn21612129
dc.identifier.urihttps://repositorio.unab.cl/xmlui/handle/ria/24246
dc.language.isoenes
dc.publisherAmerican Society for Microbiologyes
dc.rights.licenseCC BY 4.0
dc.subjectToxin-Antitoxin Systemses
dc.subjectAntitoxinses
dc.subjectAnti-Bacterial Agentses
dc.subjectAntibioticses
dc.subjectcAMPes
dc.subjectDormancyes
dc.subjectOxidative stresses
dc.subjectPersister cellses
dc.subjectSOS responsees
dc.subjectTn-Seqes
dc.titleCyclic AMP regulates bacterial persistence through repression of the oxidative stress response and SOS-dependent DNA repair in uropathogenic Escherichia colies
dc.typeArtículoes
Archivos
Bloque original
Mostrando 1 - 1 de 1
Miniatura
Nombre:
Molina_R_Cyclic_AMP_2018.pdf
Tamaño:
801.04 KB
Formato:
Adobe Portable Document Format
Descripción:
TEXTO COMPLETO EN INGLÉS
Descargar
Bloque de licencias
Mostrando 1 - 1 de 1
No hay miniatura disponible
Nombre:
license.txt
Tamaño:
1.71 KB
Formato:
Item-specific license agreed upon to submission
Descripción:
Descargar
Colecciones
FM - Artículos de Revista