Association of different mobile elements to generate novel integrative elements

Rice, Louis B.

doi:10.1007/s000180200002

Cited by 31 publications

(15 citation statements)

References 44 publications

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“…Additionally, they can incorporate into each other, which is an efficient method for accumulating resistance genes and improving their characteristics (122). Integration of an IS into a transposon may change the expression of genes in this transposon, and recombination at IS sites within or between transposons creates new elements.…”

Section: Mobile Elementsmentioning

confidence: 99%

Bacterial Genome Instability

Darmon

Leach

2014

Microbiol Mol Biol Rev

348

289

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SUMMARY Bacterial genomes are remarkably stable from one generation to the next but are plastic on an evolutionary time scale, substantially shaped by horizontal gene transfer, genome rearrangement, and the activities of mobile DNA elements. This implies the existence of a delicate balance between the maintenance of genome stability and the tolerance of genome instability. In this review, we describe the specialized genetic elements and the endogenous processes that contribute to genome instability. We then discuss the consequences of genome instability at the physiological level, where cells have harnessed instability to mediate phase and antigenic variation, and at the evolutionary level, where horizontal gene transfer has played an important role. Indeed, this ability to share DNA sequences has played a major part in the evolution of life on Earth. The evolutionary plasticity of bacterial genomes, coupled with the vast numbers of bacteria on the planet, substantially limits our ability to control disease.

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Section: Mobile Elementsmentioning

confidence: 99%

Bacterial Genome Instability

Darmon

Leach

2014

Microbiol Mol Biol Rev

348

289

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“…Besides the considerable impact that they have on the mobility and spread of antibiotic resistance genes when they make up composite transposons (31,81,146,219), insertion sequences (ISs) as single elements may also exert noticeable effects on the expression of these genes either directly, by influencing the level of their transcription, or in various ways indirectly, by affecting genes involved in their regulation or in the modulation of resistance levels. Together with the integrons, which are natural expression vectors with the capacity to capture resistance genes (95, 227), they constitute two groups of genetic elements with the potential to contribute much to high-level and multiple-antibiotic resistance in clinical isolates.…”

Section: Role Of Is Elements and Integrons In The Modulation Of Resismentioning

confidence: 99%

Modes and Modulations of Antibiotic Resistance Gene Expression

et al. 2007

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SUMMARY Since antibiotic resistance usually affords a gain of function, there is an associated biological cost resulting in a loss of fitness of the bacterial host. Considering that antibiotic resistance is most often only transiently advantageous to bacteria, an efficient and elegant way for them to escape the lethal action of drugs is the alteration of resistance gene expression. It appears that expression of bacterial resistance to antibiotics is frequently regulated, which indicates that modulation of gene expression probably reflects a good compromise between energy saving and adjustment to a rapidly evolving environment. Modulation of gene expression can occur at the transcriptional or translational level following mutations or the movement of mobile genetic elements and may involve induction by the antibiotic. In the latter case, the antibiotic can have a triple activity: as an antibacterial agent, as an inducer of resistance to itself, and as an inducer of the dissemination of resistance determinants. We will review certain mechanisms, all reversible, that bacteria have elaborated to achieve antibiotic resistance by the fine-tuning of the expression of genetic information.

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“…[1] These elements provide an efficient mechanism for rapid horizontal and vertical dissemination of antibiotic resistance determinants among bacterial species. [2][3][4] Quinolones and fluoroquinolones are among the most extensively used drugs for the treatment of bacterial infections both in human and veterinary medicine. Such wide use has led to rapidly increasing bacterial resistance to this kind of antibiotics.…”

Section: Introductionmentioning

confidence: 99%

Mechanism of Binding of Fluoroquinolones to the Quinolone Resistance‐Determining Region of DNA Gyrase: Towards an Understanding of the Molecular Basis of Quinolone Resistance

et al. 2008

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We have studied the bacterial resistance to fluoroquinolones that arises as a result of mutations in the DNA gyrase target protein. Although it is known that DNA gyrase is a target of quinolone antibacterial agents, the molecular details of the quinolone-gyrase interaction remain unclear. The mode of binding of ciprofloxacin, levofloxacin, and moxifloxacin to DNA gyrase was analyzed by means of docking calculations over the surface of the QRDR of GyrA. The analysis of these binding models allows study of the resistance mechanism associated with gyrA mutations more commonly found in E. coli fluoroquinolone-resistant strains at the atomic level. Asp87 was found to be critical in the binding of these fluoroquinolones because it interacts with the positively charged nitrogens in these bactericidal drugs. The role of the other most common mutations at amino acid codon Ser83 can be explained through the contacts that the side chain of this residue establishes with fluoroquinolone molecules. Finally, our results strongly suggest that, although Arg121 has never been found to be associated with fluoroquinolone resistance, this residue makes a pivotal contribution to the binding of the antibiotic to GyrA and to defining its position in the QRDR of the enzyme.

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Association of different mobile elements to generate novel integrative elements

Cited by 31 publications

References 44 publications

Bacterial Genome Instability

Bacterial Genome Instability

Modes and Modulations of Antibiotic Resistance Gene Expression

Mechanism of Binding of Fluoroquinolones to the Quinolone Resistance‐Determining Region of DNA Gyrase: Towards an Understanding of the Molecular Basis of Quinolone Resistance

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