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牛分枝杆菌分离株中IS6110插入位点与从动物宿主向人类宿主适应性转变的关系图谱。

Mapping of IS6110 insertion sites in Mycobacterium bovis isolates in relation to adaptation from the animal to human host.

作者信息

Otal Isabel, Gomez Ana B, Kremer Kristin, de Haas Petra, García María J, Martín Carlos, van Soolingen Dick

机构信息

Departamento de Microbiología, Medicina Preventiva y Salud Pública, Universidad de Zaragoza, Zaragoza, Spain.

出版信息

Vet Microbiol. 2008 Jun 22;129(3-4):333-41. doi: 10.1016/j.vetmic.2007.11.038. Epub 2007 Dec 8.

DOI:10.1016/j.vetmic.2007.11.038
PMID:18207337
Abstract

The physiological role and impact of IS6110 insertions on the biology of Mycobacterium tuberculosis complex is not well understood. Insertion of IS6110 in coding regions can cause loss of gene activity, while homologous recombination between two copies of IS6110 can result in the deletion of genes or in rearrangement of genomic regions involved. In addition to these genomic changes, IS6110 can also activate flanking genes through acting as a mobile promoter. In order to determine the possible role of IS6110 transposition in the adaptation to humans, we selected Mycobacterium bovis isolates from endogenous reactivation cases in elderly people in The Netherlands. The human isolates contained higher number of IS6110 copies in comparison to the bovine M. bovis strains. These additional integration sites of IS6110 were sequenced and analyzed. From 12 of such IS6110 insertion sites, 6 loci were located in the intergenic regions, and 6 other occurred within coding regions. IS6110 was inserted in a position where it might serve as a promoter in two cases. We conclude that IS6110 transpositions in M. bovis may be a driving force in the adaptation from the animal to the human host.

摘要

IS6110插入对结核分枝杆菌复合群生物学的生理作用及影响尚未完全明确。IS6110插入编码区可导致基因活性丧失,而两个IS6110拷贝之间的同源重组可导致基因缺失或相关基因组区域重排。除了这些基因组变化外,IS6110还可作为移动启动子激活侧翼基因。为了确定IS6110转座在适应人类过程中的可能作用,我们从荷兰老年人内源性再激活病例中选取了牛分枝杆菌分离株。与牛分枝杆菌菌株相比,人类分离株中IS6110拷贝数更多。对这些IS6110的额外整合位点进行了测序和分析。在12个此类IS6110插入位点中,6个位点位于基因间区域,另外6个位于编码区内。在两例中,IS6110插入的位置可能使其发挥启动子作用。我们得出结论,牛分枝杆菌中的IS转座可能是从动物宿主适应人类宿主的驱动力。

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