Danbara H, Yoshikawa M
Mol Gen Genet. 1979 Mar 20;171(2):145-52. doi: 10.1007/BF00270000.
Tra+ and tra- derivatives of drug resistance plasmid, R100-1, were isolated by phage P1 from an Hfr donor with integrated R100-1 and then analyzed by complementation tests with tra- point mutants of Flac. Tra+ derivatives of R100-1 carrying tetracycline resistance alone and those carrying all six drug-resistrance genes could support transfer of tra- point mutants of Flac except Flac traJ, whereas all of tra- derivatives of R100-1 failed to complement any one of tra- point mutants of Flac. This suggests that these tra- derivatives of R100-1 carrying tetracycline resistance gene are deleted for all the transfer genes impaired in the Flac point mutants tested. We assume a "hot point", probably a specific base sequence similar to an IS element, at the left of the tetracycline gene (Fig. 1) becomes a transduction terminus in transduction of the integrated R100-1 by phage P1. Complementation analysis of tra- derivatives carrying five resistance genes except the tetracycline gene led us to a supposition that a gene(s), probably analogous to traJ of the F plasmid, is located on R100-1 near the tetracycline gene which plays an important regulatory role for self-transfer as well as for the complementation of tra- Flac mutants.
利用噬菌体P1从整合有R100 - 1的高频重组(Hfr)供体中分离出耐药质粒R100 - 1的Tra + 和tra - 衍生物,然后用Flac的tra - 点突变体通过互补试验进行分析。仅携带四环素抗性的R100 - 1的Tra + 衍生物以及携带所有六个耐药基因的Tra + 衍生物能够支持Flac的tra - 点突变体(Flac traJ除外)的转移,而R100 - 1的所有tra - 衍生物均无法互补Flac的任何一个tra - 点突变体。这表明,这些携带四环素抗性基因的R100 - 1的tra - 衍生物缺失了在测试的Flac点突变体中受损的所有转移基因。我们假设,在四环素基因左侧(图1)的一个“热点”,可能是一个类似于插入序列(IS)元件的特定碱基序列,在噬菌体P1转导整合的R100 - 1时成为转导终点。对携带除四环素基因外的五个抗性基因的tra - 衍生物进行的互补分析使我们推测,一个基因(可能类似于F质粒的traJ)位于R100 - 1上靠近四环素基因的位置,该基因对自我转移以及tra - Flac突变体的互补起着重要的调节作用。