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Selective and non‐selective bottlenecks as drivers of the evolution of hypermutable bacterial loci

机译:选择性和非选择性瓶颈作为高端细菌基因座的演变的驱动器

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Abstract Bottlenecks reduce the size of the gene pool within populations of all life forms with implications for their subsequent survival. Here, we examine the effects of bottlenecks on bacterial commensal‐pathogens during transmission between, and dissemination within, hosts. By reducing genetic diversity, bottlenecks may alter individual or population‐wide adaptive potential. A diverse range of hypermutable mechanisms have evolved in infectious agents that allow for rapid generation of genetic diversity in specific genomic loci as opposed to the variability arising from increased genome‐wide mutation rates. These localised hypermutable mechanisms include multi‐gene phase variation (PV) of outer membrane components, multi‐allele PV of restriction systems and recombination‐driven antigenic variation. We review selected experimental and theoretical (mathematical) models pertaining to the hypothesis that localised hypermutation (LH) compensates for fitness losses caused by bottlenecks and discuss whether bottlenecks have driven the evolution of hypermutable loci.
机译:摘要瓶颈减少了所有生命中的所有生命形式的基因库的大小,具有对其随后的生存的影响。在这里,我们在传播期间检查瓶颈对细菌共生病原体的影响,宿主的传播。通过减少遗传多样性,瓶颈可能会改变个体或人口宽的自适应潜力。不同范围的超重机制在传染性药物中已经发展,其允许快速生成特定基因组基因座中的遗传多样性,而不是从增加的基因组突变率产生的变异性。这些局部化的高端机制包括外膜组分的多基因相变(PV),限制性系统的多等位基因PV和重组驱动的抗原变异。我们回顾了与假设有关的所选实验和理论(数学)模型,该假设(LH)补偿了由瓶颈引起的健身损失,并讨论瓶颈是否驱动了超重基因座的演变。

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