Non-function of a Moloney murine leukaemia virus regulatory sequence in F9 embryonal carcinoma cells
Non-function of a Moloney murine leukaemia virus regulatory sequence in F9 embryonal carcinoma cells
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DOI：
10.1038/308470a0
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发表时间：
1984
期刊：
影响因子：
64.8
通讯作者：
E. Linney;Brian Davis;J. Overhauser;E. Chao;H. Fan
中科院分区：
文献类型：
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作者：
E. Linney;Brian Davis;J. Overhauser;E. Chao;H. Fan
莫洛尼海洋白血病病毒（M-MuLV）感染胚胎癌（EC）细胞导致前病毒DNA整合到宿主细胞基因组中1 - 3，但不产生病毒1 - 6。EC细胞中缺乏病毒基因表达的一种解释是整合的病毒DNA1的甲基化。然而，随后的报道表明，M-MuLV DNA的整合发生在感染后不久，但病毒DNA甲基化发生得相当晚2，3。然而，即使在早期也没有观察到病毒基因表达。一种可能的解释是某些M-MuLV调节序列在EC细胞中不起作用。我们现在提出的证据支持这一假设。
Moloney marine leukaemia virus (M-MuLV) infection of embryonal carcinoma (EC) cells results in the integration of proviral DNA into the host cell genome1–3, but not in virus production1–6. One suggested explanation for the lack of viral gene expression in EC cells has been methylation of the integrated viral DNA1. However, subsequent reports indicated that integration of the M-MuLV DNA occurs soon after infection, but that viral DNA methylation occurs considerably later2,3. 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.