Norton J D, Connor J, Avery R J
Nucleic Acids Res. 1984 Sep 11;12(17):6839-52. doi: 10.1093/nar/12.17.6839.
The genome of Kirsten murine sarcoma virus was formed by recombination between Kirsten murine leukaemia virus sequences, and rat sequences derived from a retrovirus-like '30S' (VL30) genetic element encompassing the Kras oncogene. Using cloned DNAs we have determined the nucleotide sequences of the long terminal repeats and adjacent regions, extending across the points of recombination on the sarcoma and leukaemia virus genomes. Our results suggest that discrete regions of homology and other cryptic sequence features, may have constituted recombinational hot-spots involved in the genesis of the Kirsten murine sarcoma virus genome. We have also compared the sequence of the Kirsten murine leukaemia virus p15 env and adjacent long terminal repeat with the corresponding regions of the AKV and Gross A murine leukaemia virus genomes. This comparison has identified a leukaemogenic determinant in the U3 domain of the long terminal repeat, possibly within a enhancer-like sequence element.
柯斯顿鼠肉瘤病毒的基因组是由柯斯顿鼠白血病病毒序列与源自包含Kras癌基因的逆转录病毒样“30S”(VL30)遗传元件的大鼠序列之间的重组形成的。利用克隆的DNA,我们确定了长末端重复序列及其相邻区域的核苷酸序列,这些区域跨越了肉瘤病毒和白血病病毒基因组上的重组点。我们的结果表明,离散的同源区域和其他隐蔽的序列特征,可能构成了参与柯斯顿鼠肉瘤病毒基因组起源的重组热点。我们还将柯斯顿鼠白血病病毒p15 env和相邻的长末端重复序列的序列与AKV和格罗斯A鼠白血病病毒基因组的相应区域进行了比较。这种比较在长末端重复序列的U3结构域中确定了一个白血病致病决定因素,可能在一个类似增强子的序列元件内。