Peng F, Bradley G, Tanaka A, Lancz G, Nonoyama M
Laboratory of Virology, Tampa Bay Research Institute, St. Petersburg, Florida 33716.
J Virol. 1992 Dec;66(12):7389-96. doi: 10.1128/JVI.66.12.7389-7396.1992.
It has been reported that loss of the tumorigenic potential of attenuated Marek's disease virus (MDV) is strongly associated with amplification of the 132-bp repeat sequences found within the BamHI-D and BamHI-H fragments contained within the long terminal repeat and the long internal repeat, respectively. The expansion of this region results in loss of transcripts that are 3.8, 3.0, and 1.8 kbp long that are produced by tumorigenic strains of MDV. This evidence suggests that production of one or more of these three RNAs is strongly associated with the tumorigenic potential of the virus. In this study, we have cloned and sequenced 1.69-, 1.5-, 1.9-, and 2.2-kbp cDNAs from the BamHI-H gene family RNAs associated with tumorigenicity. The 1.69- and 2.2-kbp cDNAs are derived from nonspliced transcripts, whereas the 1.5- and 1.9-kbp cDNAs are from single spliced mRNAs spanning the BamHI-H and BamHI-I2 fragments of MDV DNA. Sequence analysis has shown two potential open reading frames in each of the cDNAs. The putative 63-amino-acid protein encoded by the first open reading frame in the 1.69-kbp cDNA and a putative 75-amino-acid protein encoded by the first open reading frame in the 1.5-kbp cDNA showed limited homology with the mouse T-cell lymphoma oncogene and the fes/fps family of kinase-related transforming proteins.
据报道,减毒马立克氏病病毒(MDV)致瘤潜力的丧失与分别位于长末端重复序列和长内部重复序列中的BamHI-D和BamHI-H片段内发现的132 bp重复序列的扩增密切相关。该区域的扩增导致MDV致瘤毒株产生的长度为3.8、3.0和1.8 kbp的转录本缺失。这一证据表明,这三种RNA中的一种或多种的产生与病毒的致瘤潜力密切相关。在本研究中,我们从与致瘤性相关的BamHI-H基因家族RNA中克隆并测序了1.69 kb、1.5 kb、1.9 kb和2.2 kb的cDNA。1.69 kb和2.2 kb的cDNA来源于未剪接的转录本,而1.5 kb和1.9 kb的cDNA来源于跨越MDV DNA的BamHI-H和BamHI-I2片段的单剪接mRNA。序列分析表明,每个cDNA中都有两个潜在的开放阅读框。1.69 kb cDNA中第一个开放阅读框编码的推定63个氨基酸的蛋白质和1.5 kb cDNA中第一个开放阅读框编码的推定75个氨基酸的蛋白质与小鼠T细胞淋巴瘤癌基因以及激酶相关转化蛋白的fes/fps家族显示出有限的同源性。