Nobusato A, Uchiyama I, Ohashi S, Kobayashi I
Institute of Medical Science, University of Tokyo, Shirokanedai, Tokyo 108-8639, Japan.
Gene. 2000 Dec 23;259(1-2):99-108. doi: 10.1016/s0378-1119(00)00456-x.
The complete genome sequences of two closely related organisms--two Helicobacter pylori strains--have recently become available. Comparison of these genomes at single base pair level has suggested the presence of a mechanism for bacterial gene mobility--insertion with long target duplications. This mechanism is formally similar to classical transposon insertion, but the duplication is much longer, often in the range of 100bp. Restriction and/or modification enzyme genes are often within or adjacent to the insertion. A similar process may have mediated insertion of the cag(+) pathogenicity island in H. pylori. A similar structure was identified in comparisons between Neisseria meningitidis and Neisseria gonorrhoeae genomes. We hypothesize that this mechanism, as well as two other types of polymorphism linked with restriction-modification genes (insertion accompanied by target deletion and a tripartite structure composed of substitution/inversion/deletion), have resulted from attack by restriction enzymes on the chromosome.
最近已获得两种密切相关生物——两种幽门螺杆菌菌株——的完整基因组序列。在单碱基对水平上对这些基因组进行比较表明存在一种细菌基因移动机制——伴有长靶重复序列的插入。该机制在形式上类似于经典转座子插入,但重复序列长得多,通常在100bp范围内。限制酶和/或修饰酶基因常常位于插入序列内部或其附近。类似的过程可能介导了幽门螺杆菌中cag(+)致病岛的插入。在脑膜炎奈瑟菌和淋病奈瑟菌基因组的比较中也发现了类似的结构。我们推测,这种机制以及与限制修饰基因相关的其他两种多态性类型(伴有靶序列缺失的插入以及由替换/倒位/缺失组成的三联体结构)是由限制酶对染色体的攻击导致的。