McClements W L, Enquist L W, Oskarsson M, Sullivan M, Vande Woude G F
J Virol. 1980 Aug;35(2):488-97. doi: 10.1128/JVI.35.2.488-497.1980.
Stocks of hybrid lambda phages carrying the complete integrated provirus of either m1 or HT1 Moloney murine sarcoma virus, as well as flanking host sequences, frequently contain significant numbers of phages carrying a specific deletion. This deletion arises from a recombination event between the terminally repeated sequences in the provirus that deletes the unique Moloney murine sarcoma virus sequences bracketed by the terminally repeated sequences. Physical mapping has shown that the deletion phage retains one complete copy of the terminally repeated sequence and the flanking mink host sequences. One such deletion, lambdaHT1r+, was used to characterize a mink genomic DNA sequence that contains an HT1 Moloney murine sarcoma virus integration site. This integration site sequence from normal mink cells was also cloned into phage lambda. An analysis of the heteroduplexes between the integration site and the lambdaHT1r+ deletion indicated that no major rearrangement of host sequences occurred upon integration of the Moloney murine sarcoma provirus.
携带m1或HT1莫洛尼鼠肉瘤病毒完整整合前病毒以及侧翼宿主序列的杂交λ噬菌体库，常常含有大量携带特定缺失的噬菌体。这种缺失源于前病毒末端重复序列之间的重组事件，该事件删除了由末端重复序列包围的独特莫洛尼鼠肉瘤病毒序列。物理图谱显示，缺失噬菌体保留了末端重复序列的一个完整拷贝以及侧翼水貂宿主序列。一种这样的缺失噬菌体λHT1r+，被用于鉴定一个包含HT1莫洛尼鼠肉瘤病毒整合位点的水貂基因组DNA序列。来自正常水貂细胞的这个整合位点序列也被克隆到λ噬菌体中。对整合位点与λHT1r+缺失之间的异源双链体的分析表明，莫洛尼鼠肉瘤前病毒整合时宿主序列未发生重大重排。
