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| Nome: | Descrição: | Tamanho: | Formato: | |
|---|---|---|---|---|
| Review | 1.03 MB | Adobe PDF |
Orientador(es)
Resumo(s)
Antibiotics target essential cellular functions but bacteria can become resistant by acquiring either exogenous resistance genes or chromosomal mutations. Resistance mutations typically occur in genes encoding essential functions; these mutations are therefore generally detrimental in the absence of drugs. However, bacteria can reduce this handicap by acquiring additional mutations, known as compensatory mutations. Genetic interactions (epistasis) either with the background or between resistances (in multiresistant bacteria) dramatically affect the fitness cost of antibiotic resistance and its compensation, therefore shaping dissemination of antibiotic resistance mutations. This Review summarizes current knowledge on the evolutionary mechanisms influencing maintenance of resistance mediated by chromosomal mutations, focusing on their fitness cost, compensatory evolution, epistasis, and the effect of the environment on these processes.
Descrição
The deposited review is a post-print version and has been submitted to peer review.
This publication hasn't any creative commons license associated.
This deposit is composed by the review, and it hasn't any supplementary materials associated.
The publication deposited was in a state of Epub Ahead of Print, at the time when the upload was made.
This publication hasn't any creative commons license associated.
This deposit is composed by the review, and it hasn't any supplementary materials associated.
The publication deposited was in a state of Epub Ahead of Print, at the time when the upload was made.
Palavras-chave
antibiotic evolution fitness costs compensation epistasis multidrug resistance
Contexto Educativo
Citação
Paulo Durão, Roberto Balbontín, Isabel Gordo, Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance, Trends in Microbiology,2018,https://doi.org/10.1016/j.tim.2018.01.005. (http://www.sciencedirect.com/science/article/pii/S0966842X18300179)