Jenkins F J, Howett M K, Rapp F
J Virol. 1983 Jan;45(1):478-81. doi: 10.1128/JVI.45.1.478-481.1983.
Insertion of HindIII DNA fragments into the HindIII site of plasmid pACYC184 destroys the promoter of the plasmid tetracycline resistance gene and causes Escherichia coli cells harboring recombinant plasmids to be tetracycline sensitive and chloramphenicol resistant. The HindIII-C DNA fragment of simian virus 40 contains the two virus promoters and the virus origin of replication. We report the isolation of recombinant plasmids that contained the simian virus 40 HindIII-C DNA fragment at the HindIII site but were capable of conferring tetracycline resistance to E. coli cells. The viral promoter sequences contained in the HindIII-C fragment presumably replaced the inactivated tetracycline resistance gene promoter sequences and enabled transcription of the tetracycline resistance gene.
将HindIII DNA片段插入质粒pACYC184的HindIII位点会破坏质粒四环素抗性基因的启动子,并使携带重组质粒的大肠杆菌细胞对四环素敏感但对氯霉素有抗性。猴病毒40的HindIII-C DNA片段包含两个病毒启动子和病毒复制起点。我们报告了在HindIII位点含有猴病毒40 HindIII-C DNA片段但能够赋予大肠杆菌细胞四环素抗性的重组质粒的分离。HindIII-C片段中包含的病毒启动子序列大概取代了失活的四环素抗性基因启动子序列,并使四环素抗性基因得以转录。