Castaneda-Garcia A.,Institute Biomedicina Of Seville |
Castaneda-Garcia A.,University of Sussex |
Prieto A.I.,Institute Biomedicina Of Seville |
Rodriguez-Beltran J.,Institute Biomedicina Of Seville |
And 17 more authors.
Nature Communications | Year: 2017
Mismatch repair (MMR) is a near ubiquitous pathway, essential for the maintenance of genome stability. Members of the MutS and MutL protein families perform key steps in mismatch correction. Despite the major importance of this repair pathway, MutS-MutL are absent in almost all Actinobacteria and many Archaea. However, these organisms exhibit rates and spectra of spontaneous mutations similar to MMR-bearing species, suggesting the existence of an alternative to the canonical MutS-MutL-based MMR. Here we report that Mycobacterium smegmatis NucS/EndoMS, a putative endonuclease with no structural homology to known MMR factors, is required for mutation avoidance and anti-recombination, hallmarks of the canonical MMR. Furthermore, phenotypic analysis of naturally occurring polymorphic NucS in a M. smegmatis surrogate model, suggests the existence of M. tuberculosis mutator strains. The phylogenetic analysis of NucS indicates a complex evolutionary process leading to a disperse distribution pattern in prokaryotes. Together, these findings indicate that distinct pathways for MMR have evolved at least twice in nature. © 2017 The Author(s).
Valencia E.Y.,University of Sao Paulo |
Esposito F.,University of Sao Paulo |
Spira B.,University of Sao Paulo |
Blazquez J.,Institute Biomedicina Of Seville Ibis Csic |
And 2 more authors.
Antimicrobial Agents and Chemotherapy | Year: 2017
Resistance to antibiotics is a global health problem. Activation of the SOS response, and the subsequent elevation in mutagenesis, contributes to the appearance of resistance mutations. Among currently used drugs, quinolones are the most potent inducers of the SOS response. In the present study, we show that amikacin inhibits ciprofloxacin-mediated SOS induction and mutagenesis in Pseudomonas aeruginosa. © 2017 American Society for Microbiology. All Rights Reserved.
Rodriguez-Beltran J.,Institute Biomedicina Of Seville Ibis Csic |
Rodriguez-Beltran J.,CSIC - National Center for Biotechnology |
Tourret J.,French Institute of Health and Medical Research |
Tourret J.,University Paris Diderot |
And 13 more authors.
Molecular Biology and Evolution | Year: 2015
Homologous recombination promotes genetic diversity by facilitating the integration of foreign DNA and intrachromosomal gene shuffling. It has been hypothesized that if recombination is variable among strains, selection should favor higher recombination rates among pathogens, as they face additional selection pressures from host defenses. To test this hypothesis we have developed a plasmid-based method for estimating the rate of recombination independently of other factors such as DNA transfer, selective processes, and mutational interference. Our results with 160 human commensal and extraintestinal pathogenic Escherichia coli (ExPEC) isolates show that the recombinant frequencies are extremely diverse (ranging 9 orders of magnitude) and plastic (they are profoundly affected by growth in urine, a condition commonly encountered by ExPEC). We find that the frequency of recombination is biased by strain lifestyle, as ExPEC isolates display strikingly higher recombination rates than their commensal counterparts. Furthermore, the presence of virulence factors is positively associated with higher recombination frequencies. These results suggest selection for high homologous recombination capacity, which may result in a higher evolvability for pathogens compared with commensals. © The Author 2015. Published by Oxford University Press on behalf of the Society for Molecular Biology and Evolution.
PubMed | Institute Biomedicina Of Seville Ibis Csic and University of Sao Paulo
Type: | Journal: Antimicrobial agents and chemotherapy | Year: 2016
Resistance to antibiotics is a global health problem. Activation of the SOS response, and the subsequent elevation in mutagenesis, contributes to the appearance of resistance mutations. Among currently used drugs, quinolones are the most potent inducers of the SOS response. In the present study, we show that amikacin inhibits ciprofloxacin-mediated SOS induction and mutagenesis in Pseudomonas aeruginosa.