van Belkum A, Scherer S, van Alphen L, Verbrugh H
Department of Medical Microbiology & Infectious Diseases, Erasmus Medical Center Rotterdam, 3015 GD Rotterdam, The Netherlands.
Microbiol Mol Biol Rev. 1998 Jun;62(2):275-93. doi: 10.1128/MMBR.62.2.275-293.1998.
Short-sequence DNA repeat (SSR) loci can be identified in all eukaryotic and many prokaryotic genomes. These loci harbor short or long stretches of repeated nucleotide sequence motifs. DNA sequence motifs in a single locus can be identical and/or heterogeneous. SSRs are encountered in many different branches of the prokaryote kingdom. They are found in genes encoding products as diverse as microbial surface components recognizing adhesive matrix molecules and specific bacterial virulence factors such as lipopolysaccharide-modifying enzymes or adhesins. SSRs enable genetic and consequently phenotypic flexibility. SSRs function at various levels of gene expression regulation. Variations in the number of repeat units per locus or changes in the nature of the individual repeat sequences may result from recombination processes or polymerase inadequacy such as slipped-strand mispairing (SSM), either alone or in combination with DNA repair deficiencies. These rather complex phenomena can occur with relative ease, with SSM approaching a frequency of 10(-4) per bacterial cell division and allowing high-frequency genetic switching. Bacteria use this random strategy to adapt their genetic repertoire in response to selective environmental pressure. SSR-mediated variation has important implications for bacterial pathogenesis and evolutionary fitness. Molecular analysis of changes in SSRs allows epidemiological studies on the spread of pathogenic bacteria. The occurrence, evolution and function of SSRs, and the molecular methods used to analyze them are discussed in the context of responsiveness to environmental factors, bacterial pathogenicity, epidemiology, and the availability of full-genome sequences for increasing numbers of microorganisms, especially those that are medically relevant.
短序列DNA重复（SSR）位点可在所有真核生物和许多原核生物基因组中被识别。这些位点含有短的或长的重复核苷酸序列基序。单个位点中的DNA序列基序可以是相同的和/或异质的。SSRs存在于原核生物界的许多不同分支中。它们存在于编码各种产物的基因中，这些产物包括识别粘附基质分子的微生物表面成分以及特定的细菌毒力因子，如脂多糖修饰酶或粘附素。SSRs赋予遗传及随之而来的表型灵活性。SSRs在基因表达调控的各个层面发挥作用。每个位点重复单元数量的变化或单个重复序列性质的改变可能源于重组过程或聚合酶功能不足，如滑链错配（SSM），单独发生或与DNA修复缺陷共同发生。这些相当复杂的现象相对容易发生，SSM在每个细菌细胞分裂时的频率接近10^(-4)，并允许高频基因转换。细菌利用这种随机策略来调整其基因库以应对选择性环境压力。SSR介导的变异对细菌致病性和进化适应性具有重要意义。对SSRs变化的分子分析有助于对病原菌传播进行流行病学研究。本文将在对环境因素的响应、细菌致病性、流行病学以及越来越多微生物（尤其是那些与医学相关的微生物）全基因组序列可用性的背景下，讨论SSRs的发生、进化和功能，以及用于分析它们的分子方法。
