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选择和非选择瓶颈作为细菌高突变位点进化的驱动力。

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

机构信息

Department of Genetics and Genome Biology, University of Leicester, Leicester, UK.

Department of Paediatrics, University of Oxford Medical Sciences Division, John Radcliffe Hospital, Oxford, UK.

出版信息

Mol Microbiol. 2020 Mar;113(3):672-681. doi: 10.1111/mmi.14453.

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.

摘要

瓶颈会减少所有生命形式种群的基因库大小,从而影响它们的后续生存。在这里,我们研究了瓶颈对宿主间传播和宿主内传播的细菌共生病原体的影响。通过减少遗传多样性,瓶颈可能会改变个体或群体的适应潜力。在传染性病原体中已经进化出了多种高突变机制,这些机制可以在特定的基因组位点快速产生遗传多样性,而不是通过增加全基因组突变率产生的可变性。这些局部高突变机制包括外膜成分的多基因相位变异(PV)、限制系统的多等位基因 PV 和重组驱动的抗原变异。我们回顾了与局部高突变(LH)补偿瓶颈引起的适应性损失的假设相关的选定实验和理论(数学)模型,并讨论了瓶颈是否推动了高突变位点的进化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a1e4/7154626/ad1558efb45a/MMI-113-672-g001.jpg

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