Iida S, Hiestand-Nauer R, Hänni C, Arber W
Mol Gen Genet. 1985;201(2):174-7. doi: 10.1007/BF00425656.
The composite transposon Tn2672 is a derivative of the Tn3-related transposon Tn902 whose bla gene providing ampicillin resistance had been inactivated by the insertion of the IS1-flanked multiple drug resistance transposon Tn2671. Most ampicillin resistant revertants of Tn2672 are due to precise excision of Tn2671. However, a rare Bla+ revertant which still retains all the previously acquired drug resistance markers was isolated. On this revertant, the 5' part of the split bla gene on Tn2672 has converted to an intact, active bla gene, and the entire Tn902 is structurally restored. In contrast, the adjacent IS1b element belonging to Tn2671 has its terminal 142 base pairs deleted. Despite of this rearrangement, the split 3' part of bla and its adjacent sequences have remained unchanged. Models are presented to explain the observed DNA rearrangements, and their similarity with gene conversion events is discussed.
复合转座子Tn2672是与Tn3相关的转座子Tn902的衍生物,其提供氨苄青霉素抗性的bla基因因插入IS1侧翼的多重耐药转座子Tn2671而失活。Tn2672的大多数氨苄青霉素抗性回复突变体是由于Tn2671的精确切除。然而,分离出了一种罕见的Bla+回复突变体,它仍然保留了所有先前获得的耐药标记。在这个回复突变体上,Tn2672上分裂的bla基因的5'部分已转化为完整的、有活性的bla基因,并且整个Tn902在结构上得以恢复。相反,属于Tn2671的相邻IS1b元件的末端142个碱基对缺失。尽管有这种重排,bla的分裂3'部分及其相邻序列仍保持不变。本文提出了模型来解释观察到的DNA重排,并讨论了它们与基因转换事件的相似性。