生物
遗传学
适应(眼睛)
基因
宿主适应
体细胞突变
计算生物学
毒力
抗体
神经科学
B细胞
作者
Richard Moxon,Christopher D. Bayliss,Derek W. Hood
出处
期刊:Annual Review of Genetics
[Annual Reviews]
日期:2006-12-01
卷期号:40 (1): 307-333
被引量:413
标识
DOI:10.1146/annurev.genet.40.110405.090442
摘要
Bacterial pathogens face stringent challenges to their survival because of the many unpredictable, often precipitate, and dynamic changes that occur in the host environment or in the process of transmission from one host to another. Bacterial adaptation to their hosts involves either a mechanism for sensing and responding to external changes or the selection of variants that arise through mutation. Here we review how bacterial pathogens exploit localized hypermutation, through polymerase slippage of simple sequence repeats (SSRs), to generate phenotypic variation and enhanced fitness. These SSRs are located within the reading frame or in the promoter of a subset of genes, often termed contingency loci, whose functions are usually involved in direct interactions with host structures.
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