Linney E, Davis B, Overhauser J, Chao E, Fan H
Nature. 1984;308(5958):470-2. doi: 10.1038/308470a0.
Moloney murine leukaemia virus (M-MuLV) infection of embryonal carcinoma (EC) cells results in the integration of proviral DNA into the host cell genome, but not in virus production. One suggested explanation for the lack of viral gene expression in EC cells has been methylation of the integrated viral DNA. However, subsequent reports indicated that integration of the M-MuLV DNA occurs soon after infection, but that viral DNA methylation occurs considerably later. Nevertheless, viral gene expression is not observed even at early times. One possible explanation is that certain M-MuLV regulatory sequences do not function in EC cells. We now present evidence which supports this hypothesis.
莫洛尼鼠白血病病毒(M-MuLV)感染胚胎癌细胞(EC)会导致前病毒DNA整合到宿主细胞基因组中,但不会产生病毒。对于EC细胞中缺乏病毒基因表达,一种提出的解释是整合的病毒DNA发生了甲基化。然而,随后的报告表明,M-MuLV DNA在感染后不久就发生整合,但病毒DNA甲基化则要晚得多。尽管如此,即使在早期也未观察到病毒基因表达。一种可能的解释是某些M-MuLV调控序列在EC细胞中不起作用。我们现在提供支持这一假设的证据。