Nishizawa M, Koyama T, Kawai S
J Virol. 1985 Sep;55(3):881-5. doi: 10.1128/JVI.55.3.881-885.1985.
TK15, a mutant derived from a temperature-sensitive mutant of Rous sarcoma virus (tsNY68), has extremely low infectivity although it has intact viral genes. Biological and biochemical analyses of the virus and virus-induced transformants showed that the mutant has a defect in the packaging of its own genomic RNA possibly owing to a deletion near the 5' end (S. Kawai and T. Koyama, J. Virol. 51:147-153, 1984; T. Koyama, F. Harada, and S. Kawai, J. Virol. 51:154-162, 1984). Nucleotide sequence analysis of the provirus DNA of the mutant revealed that the deletion extends from the 3' end of the primer binding site to 22 bases upstream of the gag initiation codon and also suggested that possible binding between an extra region of the primer molecule and the viral genome resulting from the deletion causes another defect in the replication of the TK15 genome. It was suggested that the deletion of 237 bases in TK15 was generated during reverse transcription of the genome by the skipping of a sequence between identical 13-base sequences present in the primer binding site and 35 to 22 bases upstream of the gag initiation codon of the parental virus.
TK15是源自劳斯肉瘤病毒温度敏感突变体(tsNY68)的一个突变体,尽管其病毒基因完整,但感染性极低。对该病毒及其诱导的转化体进行的生物学和生化分析表明,该突变体在自身基因组RNA的包装方面存在缺陷,可能是由于5'端附近的缺失(S. Kawai和T. Koyama,《病毒学杂志》51:147 - 153,1984;T. Koyama、F. Harada和S. Kawai,《病毒学杂志》51:154 - 162,1984)。对该突变体前病毒DNA的核苷酸序列分析表明,缺失从引物结合位点的3'端延伸至gag起始密码子上游22个碱基处,并且还表明,由于缺失导致引物分子的一个额外区域与病毒基因组之间可能的结合,会造成TK15基因组复制中的另一个缺陷。有人提出,TK15中237个碱基的缺失是在基因组逆转录过程中,通过跳过亲本病毒引物结合位点中存在的相同13碱基序列与gag起始密码子上游35至22个碱基之间的一段序列而产生的。