Pecenka V, Dvorák M, Karafiát V, Trávnícek M
Institute of Molecular Genetics, Czechoslovak Academy of Sciences, Praha.
Folia Biol (Praha). 1988;34(4):215-32.
Using Southern hybridization with a series of probes derived from the MAV provirus we searched for structurally changed MAV-2 proviruses in the DNA from MAV-2-induced nephroblastomas. Anomalous fragments of MAV-2 provirus were found in all samples analysed in more detail. Comparison of the sizes of anomalous fragments detected by different probes in the same sample indicates that the fragments, at least in a majority of cases, do not represent recombinant proviruses (which might contain transduced oncogene) but deleted proviruses only. Various types of proviral deletions occur in different nephroblastoma clones, and no preferred type of deletion was found. The defects in MAV-2 sequences appear in infected chickens de novo, because defective proviruses also occur in tumours of chickens that have been infected with the plaque-purified MAV-2 preparations and, in addition, most of the proviral defects found prevent the virus from replicating and from being transmitted by infection. The regular occurrence of defective proviruses in tumour DNA supports the concept that the proviral defects are involved in oncogenesis. Hypotheses on the substance of this involvement are discussed.
我们使用一系列源自MAV前病毒的探针进行Southern杂交，在MAV - 2诱导的肾母细胞瘤的DNA中寻找结构发生改变的MAV - 2前病毒。在所有更详细分析的样本中均发现了MAV - 2前病毒的异常片段。对同一样本中不同探针检测到的异常片段大小进行比较表明，这些片段至少在大多数情况下并不代表重组前病毒（可能含有转导的癌基因），而仅为缺失的前病毒。不同类型的前病毒缺失发生在不同的肾母细胞瘤克隆中，未发现偏好的缺失类型。MAV - 2序列中的缺陷在感染鸡中是从头出现的，因为在感染了噬菌斑纯化的MAV - 2制剂的鸡的肿瘤中也存在缺陷前病毒，此外，发现的大多数前病毒缺陷会阻止病毒复制和通过感染传播。肿瘤DNA中缺陷前病毒的经常出现支持了前病毒缺陷参与肿瘤发生的概念。文中讨论了关于这种参与实质的假设。
