Your browser doesn't support javascript.
loading
Evolutionary Paths That Expand Plasmid Host-Range: Implications for Spread of Antibiotic Resistance.
Loftie-Eaton, Wesley; Yano, Hirokazu; Burleigh, Stephen; Simmons, Ryan S; Hughes, Julie M; Rogers, Linda M; Hunter, Samuel S; Settles, Matthew L; Forney, Larry J; Ponciano, José M; Top, Eva M.
Afiliação
  • Loftie-Eaton W; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Yano H; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Burleigh S; Department of Biological Sciences, University of Idaho.
  • Simmons RS; Department of Biological Sciences, University of Idaho.
  • Hughes JM; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Rogers LM; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Hunter SS; Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Settles ML; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Forney LJ; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho.
  • Ponciano JM; Department of Biology, University of Florida josemi@ufl.edu evatop@uidaho.edu.
  • Top EM; Department of Biological Sciences, University of Idaho Institute for Bioinformatics and Evolutionary Studies (IBEST), University of Idaho josemi@ufl.edu evatop@uidaho.edu.
Mol Biol Evol ; 33(4): 885-97, 2016 Apr.
Article em En | MEDLINE | ID: mdl-26668183
The World Health Organization has declared the emergence of antibiotic resistance to be a global threat to human health. Broad-host-range plasmids have a key role in causing this health crisis because they transfer multiple resistance genes to a wide range of bacteria. To limit the spread of antibiotic resistance, we need to gain insight into the mechanisms by which the host range of plasmids evolves. Although initially unstable plasmids have been shown to improve their persistence through evolution of the plasmid, the host, or both, the means by which this occurs are poorly understood. Here, we sought to identify the underlying genetic basis of expanded plasmid host-range and increased persistence of an antibiotic resistance plasmid using a combined experimental-modeling approach that included whole-genome resequencing, molecular genetics and a plasmid population dynamics model. In nine of the ten previously evolved clones, changes in host and plasmid each slightly improved plasmid persistence, but their combination resulted in a much larger improvement, which indicated positive epistasis. The only genetic change in the plasmid was the acquisition of a transposable element from a plasmid native to the Pseudomonas host used in these studies. The analysis of genetic deletions showed that the critical genes on this transposon encode a putative toxin-antitoxin (TA) and a cointegrate resolution system. As evolved plasmids were able to persist longer in multiple naïve hosts, acquisition of this transposon also expanded the plasmid's host range, which has important implications for the spread of antibiotic resistance.
Assuntos
Palavras-chave

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Plasmídeos / Pseudomonas / Resistência Microbiana a Medicamentos / Evolução Molecular Limite: Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Plasmídeos / Pseudomonas / Resistência Microbiana a Medicamentos / Evolução Molecular Limite: Humans Idioma: En Ano de publicação: 2016 Tipo de documento: Article