Berkower A S, Lilly F, Soeiro R
Cell. 1980 Mar;19(3):637-42. doi: 10.1016/s0092-8674(80)80040-7.
The regulation of expression of the Friend virus complex (FV) was studied in clones of H-2 congenic erythroleukemia cell lines. Molecular probes specific for each of the two FV components were generated and hybridized to RNA extracted from clones differing with respect to virus production or viral envelope antigen expression. Sequences representing the defective component of FV continued to be transcribed in cells regardless of virus production. The presence of helper virus-specific sequences, however, was shown to be directly related to virus expression. Molecular hybridization with cytoplasmic and nuclear RNA extracted from the H-2 congenic clones representing various stages of viral expression demonstrated a direct correlation between the level of transcription of FMuLV-specific sequences and the degree of virus expression. These data suggest that regulation of FV expression is primarily related to the cessation of helper virus transcription in the cell lines studied. In this paper we provide further evidence that the defective viral components is responsible for the rapid malignancy associated with Friend disease.
在H-2同基因红白血病细胞系的克隆中研究了弗瑞德病毒复合体(FV)的表达调控。针对FV两个组分各自产生了特异性分子探针,并与从在病毒产生或病毒包膜抗原表达方面存在差异的克隆中提取的RNA进行杂交。代表FV缺陷组分的序列在细胞中持续转录,而与病毒产生无关。然而,辅助病毒特异性序列的存在显示与病毒表达直接相关。对从代表病毒表达不同阶段的H-2同基因克隆中提取的细胞质和核RNA进行分子杂交,结果表明F-MuLV特异性序列的转录水平与病毒表达程度之间存在直接相关性。这些数据表明,在所研究的细胞系中,FV表达的调控主要与辅助病毒转录的停止有关。在本文中,我们提供了进一步的证据,证明缺陷病毒组分与弗瑞德病相关的快速恶性肿瘤有关。