Caporossi D, Bacchetti S
Department of Pathology, McMaster University, Hamilton, Ontario, Canada.
J Gen Virol. 1990 Apr;71 ( Pt 4):801-8. doi: 10.1099/0022-1317-71-4-801.
Infection of human embryonic kidney cells with adenovirus type 5 (Ad5) induces aberrations (gaps and breaks) in the cell chromosomes. We have conducted a study utilizing a large number of Ad5 mutants to identify the viral functions that are responsible for the occurrence of cytogenetic damage. The results of our investigation have indicated that expression of the gene products of the Ad5 early region 1A (E1A) is necessary for the induction of chromosomal aberrations and that other early viral gene products do not appear to contribute to this phenotype. We have also shown that expression of both the major E1A gene products, the 243 amino acid and the 289 amino acid proteins, is required for induction of damage at wild-type levels, although the 289 amino acid protein appears to retain detectable activity on its own. Lastly, we have observed that deletions in the amino-terminal region of the E1A proteins and in the transactivating domain of the 289 amino acid protein prevent the occurrence of cytogenetic damage, whereas mutations elsewhere in the proteins do not affect this process.
用人胚肾细胞感染5型腺病毒（Ad5）会诱导细胞染色体出现畸变（裂隙和断裂）。我们利用大量Ad5突变体进行了一项研究，以确定导致细胞遗传学损伤发生的病毒功能。我们的研究结果表明，Ad5早期区域1A（E1A）基因产物的表达是诱导染色体畸变所必需的，而其他早期病毒基因产物似乎对这种表型没有贡献。我们还表明，尽管289个氨基酸的蛋白质似乎自身保留了可检测到的活性，但野生型水平的损伤诱导需要主要E1A基因产物243个氨基酸和289个氨基酸蛋白质的表达。最后，我们观察到E1A蛋白质氨基末端区域和289个氨基酸蛋白质反式激活结构域的缺失会阻止细胞遗传学损伤的发生，而蛋白质其他部位的突变不会影响这一过程。
