Bender J, Kleckner N
Cell. 1986 Jun 20;45(6):801-15. doi: 10.1016/0092-8674(86)90555-6.
We present genetic evidence that the tetracycline resistance element Tn10 transposes by a nonreplicative mechanism. Heteroduplex Tn10 elements containing three single base pair mismatches were constructed on lambda phage genomes and allowed to transpose from lambda into the bacterial chromosome. Analysis of TetR colonies resulting from such transpositions suggests that information from both strands of the transposing Tn10 element is transmitted faithfully to its transposition product. The simplest interpretation of these results is that the transposing element is excised from the donor molecule and inserted into the target molecule without being replicated. A mismatch 70 base pairs from one end of the transposon is preserved, suggesting that there is little or no replication, even at the termini of the element, during transposition in vivo.
我们提供了遗传证据,表明四环素抗性元件Tn10通过非复制机制进行转座。在λ噬菌体基因组上构建了含有三个单碱基对错配的异源双链Tn10元件,并使其从λ转座到细菌染色体中。对这种转座产生的TetR菌落的分析表明,转座的Tn10元件两条链的信息都被忠实地传递到了其转座产物中。这些结果最简单的解释是,转座元件从供体分子上切除并插入到靶分子中,而没有进行复制。转座子一端70个碱基对处的错配得以保留,这表明在体内转座过程中,即使在元件的末端,也很少或没有复制。