Bouchard L, Mathieu F, Bastin M
Department of Microbiology, University of Sherbrooke, Quebec, Canada.
Oncogene. 1988 Apr;2(4):379-86.
We studied the activation of polyoma middle T expression in revertant cells carrying transcriptionally inactive copies of the middle T (pmt) oncogene. Introduction of polyoma large T with neo into a rat cell line containing multiple copies of pmt stably integrated into the genome corrected the transformation defect in some of the transfected cells by activating the resident pmt gene. However, once the cells were transformed, continuous expression of the large T protein was not required for the maintenance of pmt expression and hence the maintenance of the transformed state. Transformants arising spontaneously as well as those induced by large T exhibited frequent rearrangements of the pmt inserts. Our results suggest that large T activated pmt expression by a hit-and-run mechanism involving recombination of sequences in the viral insert.
我们研究了携带转录失活的中T（pmt）癌基因拷贝的回复细胞中多瘤病毒中T表达的激活情况。将带有新霉素抗性基因的多瘤病毒大T导入一个基因组中稳定整合有多个pmt拷贝的大鼠细胞系，通过激活内源性pmt基因，纠正了部分转染细胞的转化缺陷。然而，一旦细胞发生转化，维持pmt表达进而维持转化状态并不需要大T蛋白的持续表达。自发产生的转化体以及由大T诱导产生的转化体都频繁出现pmt插入片段的重排。我们的结果表明，大T通过一种涉及病毒插入序列重组的“打了就跑”机制激活pmt表达。
