Edbauer C, Lamberti C, Tong J, Williams J
Department of Biological Sciences, Carnegie Mellon University, Pittsburgh, Pennsylvania 15213-3890.
J Virol. 1988 Sep;62(9):3265-73. doi: 10.1128/JVI.62.9.3265-3273.1988.
The adenovirus type 12 mutants in700 and pm700 carry site-specific mutations within the reading frame encoding the E1B 19-kilodalton protein (19K protein) which prevent the production of the intact 19K protein. In cultures of human A549 cells, these mutants grow just as well as the wild-type virus does, but they display a large-plaque (lp), cytocidal (cyt) phenotype. DNA in these infected cells is not degraded, but at late times in human KB cells infected by the mutants, the mutants display a DNA degradation (deg) phenotype. The transformation phenotype of these mutants is also host range. Although the mutants are defective for transformation of the 3Y1 rat cell line, they transform rat and mouse primary kidney cells in vitro at wild-type efficiency and are capable of inducing tumors in rats. These results support the view that the type 12 E1B 19K protein is not obligatory for oncogenic transformation.
腺病毒12型突变体in700和pm700在编码E1B 19千道尔顿蛋白(19K蛋白)的阅读框内携带位点特异性突变,这些突变阻止了完整19K蛋白的产生。在人A549细胞培养物中,这些突变体的生长与野生型病毒一样好,但它们表现出大斑块(lp)、杀细胞(cyt)表型。这些受感染细胞中的DNA未被降解,但在被这些突变体感染的人KB细胞的后期,突变体表现出DNA降解(deg)表型。这些突变体的转化表型也具有宿主范围。虽然这些突变体对3Y1大鼠细胞系的转化有缺陷,但它们能以野生型效率在体外转化大鼠和小鼠原代肾细胞,并能够在大鼠体内诱导肿瘤。这些结果支持了12型E1B 19K蛋白对于致癌转化不是必需的这一观点。