Chandler M, de la Tour E B, Willems D, Caro L
Mol Gen Genet. 1979 Oct 3;176(2):221-31. doi: 10.1007/BF00273216.
We have isolated variants of the plasmid RTF which have received the transposon Tn9 from bacteriophage P1Cm. We have shown by the formation of heteroduplex molecules between one RTF:Tn9 derivative and R100.1 that Tn9 is homologous to the r-determinant region of R100.1 which carries the determinants for chloramphenicol resistance. This suggests that Tn9 was derived from an r-det like structure by deletion, possibly mediated by one of the flanking IS1 elements. In spite of the similarity in structure between Tn9 and r-det however, we have demonstrated two distinct differences in the behavior of these two elements: 1) Tn9 but not r-det, is able to amplify, by a recA dependent mechanism, when cells harboring RTF::Tn9 are grown in the presence of chloramphenicol, and 2) Tn9, unlike r-det, does not form extrachromosomal circular molecules when RTF::Tn9 is tegrated into the bacterial chromosome.
我们已经分离出了质粒RTF的变体，这些变体从噬菌体P1Cm获得了转座子Tn9。我们通过在一种RTF:Tn9衍生物与R100.1之间形成异源双链分子表明，Tn9与R100.1的r-决定簇区域同源，该区域携带氯霉素抗性决定簇。这表明Tn9可能是由侧翼IS1元件之一介导的缺失，从一个类似r-决定簇的结构衍生而来。然而，尽管Tn9与r-决定簇在结构上相似，我们已经证明了这两个元件在行为上有两个明显的差异：1）当携带RTF::Tn9的细胞在氯霉素存在下生长时，Tn9能够通过一种recA依赖性机制进行扩增，而r-决定簇则不能；2）与r-决定簇不同，当RTF::Tn9整合到细菌染色体中时，Tn9不会形成染色体外环状分子。
