Sampson S L, Warren R M, Richardson M, Victor T C, Jordaan A M, van der Spuy G D, van Helden P D
MRC Centre for Molecular and Cellular Biology, Department of Medical Biochemistry, Faculty of Health Sciences, Stellenbosch University, Tygerberg 7505, South Africa.
J Bacteriol. 2003 May;185(9):2856-66. doi: 10.1128/JB.185.9.2856-2866.2003.
This study investigates the phenomenon of IS6110-mediated deletion polymorphism in the direct repeat (DR) region of the genome of Mycobacterium tuberculosis. Clinical isolates and their putative predecessors were compared using a combination of DR region restriction fragment length polymorphism, IS6110 DNA fingerprinting, spoligotyping, and DNA sequencing, which allowed the mapping of chromosome structure and deletion junctions. The data suggest that adjacently situated IS6110 elements mediate genome deletion. However, in contrast to previous reports, deletions appear to be mediated by inversely oriented IS6110 elements. This suggests that these events may occur via mechanisms other than RecA-mediated homologous recombination. The results underscore the important role of IS6110-associated deletion hypervariability in driving M. tuberculosis genome evolution.
本研究调查了结核分枝杆菌基因组直接重复（DR）区域中IS6110介导的缺失多态性现象。使用DR区域限制性片段长度多态性、IS6110 DNA指纹图谱、间隔寡核苷酸分型（spoligotyping）和DNA测序相结合的方法，对临床分离株及其假定的祖先进行了比较，这使得能够绘制染色体结构和缺失连接点。数据表明，相邻的IS6110元件介导基因组缺失。然而，与之前的报道相反，缺失似乎是由反向排列的IS6110元件介导的。这表明这些事件可能通过RecA介导的同源重组以外的机制发生。结果强调了IS6110相关缺失高变异性在驱动结核分枝杆菌基因组进化中的重要作用。
