Shiroki K, Saito I, Maruyama K, Shimojo H
J Virol. 1983 May;46(2):632-7. doi: 10.1128/JVI.46.2.632-637.1983.
A nondefective recombinant between adenovirus type 5 (Ad5) and type 12 (Ad12), rc-1 (Ad5 dl312, carrying the Ad12 E1A gene), was isolated from hamster cell foci transformed by a defective recombinant, rcB-1 (dl312, carrying the Ad12 E1 gene). The recombinant rc-1 grew in human embryo kidney and KB cells in the absence of helper and synthesized Ad12 T antigen g, the product of the E1A gene. The genome of rc-1 has a deletion between 79.9 and 82.5 map units of Ad5 dl312 DNA with an insertion of 0.1 to 5.5 map units of Ad12 DNA at the deletion site. The mRNAs of Ad12 E1A were transcribed from the Ad12 E1A promoter, and unusual RNAs were abundantly transcribed from the Ad5 E3 promoter on the opposite strand. The frequency of cell transformation with rc-1 was lower than those with Ad5 and Ad12 wild types.
从由缺陷重组体rcB-1(dl312,携带腺病毒12型(Ad12)E1基因)转化的仓鼠细胞灶中分离出腺病毒5型(Ad5)和12型(Ad12)之间的无缺陷重组体rc-1(Ad5 dl312,携带Ad12 E1A基因)。重组体rc-1在无辅助病毒的情况下能在人胚肾细胞和KB细胞中生长,并合成Ad12 T抗原g,即E1A基因的产物。rc-1的基因组在Ad5 dl312 DNA的79.9至82.5图谱单位之间有一个缺失,在缺失位点插入了0.1至5.5图谱单位的Ad12 DNA。Ad12 E1A的mRNA从Ad12 E1A启动子转录而来,相反链上的Ad5 E3启动子大量转录出异常RNA。rc-1诱导细胞转化的频率低于Ad5和Ad12野生型。