A variant of CRPV DNA preferentially maintained as a plasmid in NIH 3T3 cells and characterization of its transcripts in nude mouse tumors.
A variant of CRPV DNA preferentially maintained as a plasmid in NIH 3T3 cells and characterization of its transcripts in nude mouse tumors.
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CRPV DNA 的变体在 NIH 3T3 细胞中优先维持为质粒，并在裸鼠肿瘤中表征其转录物。
DOI：
10.1016/0042-6822(87)90149-8
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发表时间：
1987
期刊：
影响因子：
3.7
通讯作者：
Wettstein,FO
中科院分区：
文献类型：
--
作者：
Nasseri,M;Wettstein,FO
兔和人乳头瘤病毒是严格嗜上皮的，它们的DNA在其天然宿主的良性病变（疣）中进行染色体外复制。它们的组织和宿主特异性被认为是遗传控制的，并且可能是转化异源细胞效率低下的原因。在我们的研究中，CRPV DNA在NIH 3T3细胞中没有诱导病灶，在与选择标记的共转染中只发现整合的DNA，病毒DNA似乎没有转录活性，因为没有检测到转录本，并且在细胞中对裸鼠没有致瘤性。与这些结果相反，自发衍生的CRPV变体DNA能够在染色体外复制，并且大多数病灶衍生的细胞系对裸鼠具有致瘤性。在裸小鼠肿瘤中，变异DNA仅保留在染色体外，并检测到病毒转录本。主要转录本的大小为2.0和1.3 kb，这表明E6和E7被表达。在兔组织中的情况是不同的，无论是变异和野生型DNA保持extrachromosomally。在小鼠细胞中，该变异体的染色体外维持，而野生型DNA的染色体外维持，表明该变异体缺乏可能在CRPV的宿主和组织限制中发挥作用的序列。变异DNA中的缺失位于晚期区域，包括L1的大部分或全部和L2的羧基末端区段。第二个缺失消除了一些pBR322序列。
Rabbit and human papillomaviruses are strictly epitheliotropic and their DNA replicates extrachromosomally in benign lesions (warts) of their natural host. Their tissue and host specificity is thought to be genetically controlled and may account for the inefficiency in transforming heterologous cells. In our hands, CRPV DNA did not induce foci in NIH 3T3 cells and in cotransfections with a selectable marker only integrated DNA was found. The viral DNA appeared to be transcriptionally inactive since no transcripts could be detected and in cells were not tumorigenic for nude mice. In contrast to these results a spontaneously derived CRPV variant DNA was able to replicate extrachromosomally and a majority of focus-derived cell lines were tumorigenic for nude mice. In nude mouse tumors the variant DNA remained exclusively extrachromosomal and viral transcripts were detected. The sizes of the major transcripts were 2.0 and 1.3 kb and this suggested that E6 and E7 were expressed. The situation in rabbit tissue was different; both variant and wild-type DNA were maintained extrachromosomally. The extrachromosomal maintenance of the variant but not of wild-type DNA in mouse cells suggests that the variant lacks sequences which may play a role in the host and the tissue restriction of CRPV. The deletion in the variant DNA was located in the late region and included most or all of L1 and a carboxy terminal segment of L2. A second deletion eliminated some pBR322 sequences.