FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2786822213> ?p ?o ?g. }

• W2786822213 endingPage "691" @default.
• W2786822213 startingPage "677" @default.
• W2786822213 abstract "Most antibiotic resistance mutations reduce bacterial fitness in the absence of the antibiotic, but some are not costly, or can even be advantageous in certain environments, including infection-related conditions. Acquiring a new resistance can alleviate the cost of a pre-existing one, thus favouring the emergence of multidrug-resistant bacteria. The compensatory evolution of multidrug-resistant bacteria is distinct from that of single-resistant bacteria, since the proteins mediating functional interactions between those affected by resistance mutations become new targets for their compensation. 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. 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. an inheritable ability of microorganisms to grow at high concentrations of antibiotic (independently of whether it is bacteriostatic or bactericidal) and irrespective of the duration of treatment. adaptive mutations which reduce the fitness costs caused by a pre-existing condition, such as the presence of antibiotic resistance mutations or MRE. deleterious effect on an organism’s fitness caused by the presence of either a chromosomal mutation conferring resistance or mobile genetic elements carrying resistance. a phenomenon in which the effect of one mutation is dependent on the presence of other pre-existing mutations, for example, the genetic background. a term that refers to the survival and reproductive success of an organism in an environment. In bacteria relative fitness is measured by competing two genotypes (i.e., resistant versus sensitive) and accounting for the change in frequency over time (competitive fitness). Fitness of bacteria can also be estimated by measuring reproduction-related traits, such as growth rate, carrying capacity, or length of lag phase. evolutionary process by which the genotypes best phenotypically adapted to a particular environment in a population increase in relative frequency with respect to less-adapted organisms over generations. genetic reversion occurs when a mutation returns to the original genetic sequence. Phenotypic reversion of an AR mutation occurs when the resistance mutation is maintained but the sensitive phenotype is restored. an evolutionary effect exerted by any cause or agent (i.e., an antibiotic) that increases or reduces the reproductive success (fitness) of a genotype, changing its frequency in a population." @default.
• W2786822213 created "2018-02-23" @default.
• W2786822213 creator A5026732169 @default.
• W2786822213 creator A5049923424 @default.
• W2786822213 creator A5091837645 @default.
• W2786822213 date "2018-08-01" @default.
• W2786822213 modified "2023-10-16" @default.
• W2786822213 title "Evolutionary Mechanisms Shaping the Maintenance of Antibiotic Resistance" @default.
• W2786822213 cites W1510121895 @default.
• W2786822213 cites W1608826984 @default.
• W2786822213 cites W1794788760 @default.
• W2786822213 cites W1890987455 @default.
• W2786822213 cites W1922732464 @default.
• W2786822213 cites W1964171417 @default.
• W2786822213 cites W1964529071 @default.
• W2786822213 cites W1967120694 @default.
• W2786822213 cites W1967778991 @default.
• W2786822213 cites W1971154088 @default.
• W2786822213 cites W1971724552 @default.
• W2786822213 cites W1974227993 @default.
• W2786822213 cites W1975675040 @default.
• W2786822213 cites W1978772598 @default.
• W2786822213 cites W1980357487 @default.
• W2786822213 cites W1980588572 @default.
• W2786822213 cites W1981214207 @default.
• W2786822213 cites W1984664666 @default.
• W2786822213 cites W1995025557 @default.
• W2786822213 cites W1995176570 @default.
• W2786822213 cites W1997078773 @default.
• W2786822213 cites W1997152162 @default.
• W2786822213 cites W1999699598 @default.
• W2786822213 cites W2004960255 @default.
• W2786822213 cites W2006805047 @default.
• W2786822213 cites W2008144158 @default.
• W2786822213 cites W2009119563 @default.
• W2786822213 cites W2011197538 @default.
• W2786822213 cites W2011343696 @default.
• W2786822213 cites W2012515231 @default.
• W2786822213 cites W2012766690 @default.
• W2786822213 cites W2012980277 @default.
• W2786822213 cites W2016666153 @default.
• W2786822213 cites W2020591349 @default.
• W2786822213 cites W2027951608 @default.
• W2786822213 cites W2028789388 @default.
• W2786822213 cites W2028800939 @default.
• W2786822213 cites W2031141619 @default.
• W2786822213 cites W2036978592 @default.
• W2786822213 cites W2037212291 @default.
• W2786822213 cites W2040609055 @default.
• W2786822213 cites W2041949408 @default.
• W2786822213 cites W2043887558 @default.
• W2786822213 cites W2044913918 @default.
• W2786822213 cites W2046484293 @default.
• W2786822213 cites W2046739987 @default.
• W2786822213 cites W2047152956 @default.
• W2786822213 cites W2056981303 @default.
• W2786822213 cites W2064830028 @default.
• W2786822213 cites W2066286375 @default.
• W2786822213 cites W2067136681 @default.
• W2786822213 cites W2069107501 @default.
• W2786822213 cites W2070498478 @default.
• W2786822213 cites W2072244058 @default.
• W2786822213 cites W2072498886 @default.
• W2786822213 cites W2073391367 @default.
• W2786822213 cites W2073556554 @default.
• W2786822213 cites W2075476726 @default.
• W2786822213 cites W2084895511 @default.
• W2786822213 cites W2090640084 @default.
• W2786822213 cites W2090651792 @default.
• W2786822213 cites W2092193084 @default.
• W2786822213 cites W2095222153 @default.
• W2786822213 cites W2096231326 @default.
• W2786822213 cites W2097807888 @default.
• W2786822213 cites W2099218800 @default.
• W2786822213 cites W2100799586 @default.
• W2786822213 cites W2101134401 @default.
• W2786822213 cites W2102157178 @default.
• W2786822213 cites W2105995834 @default.
• W2786822213 cites W2111500681 @default.
• W2786822213 cites W2113774740 @default.
• W2786822213 cites W2114702482 @default.
• W2786822213 cites W2115263303 @default.
• W2786822213 cites W2118609795 @default.
• W2786822213 cites W2119384132 @default.
• W2786822213 cites W2121586129 @default.
• W2786822213 cites W2123101103 @default.
• W2786822213 cites W2123832578 @default.
• W2786822213 cites W2123844970 @default.
• W2786822213 cites W2126115772 @default.
• W2786822213 cites W2126184746 @default.
• W2786822213 cites W2126532797 @default.
• W2786822213 cites W2127847106 @default.
• W2786822213 cites W2128894514 @default.
• W2786822213 cites W2131256712 @default.
• W2786822213 cites W2131322477 @default.
• W2786822213 cites W2132687294 @default.
• W2786822213 cites W2133275732 @default.
• W2786822213 cites W2135682495 @default.

• next