Hollon T, Yoshimura F K
Department of Microbiology, University of Washington, Seattle 98195.
J Virol. 1989 Aug;63(8):3353-61. doi: 10.1128/JVI.63.8.3353-3361.1989.
We have used deletion and recombinant long terminal repeat (LTR) mutants to examine enhancer activity differences between LTRs of the nonpathogenic Akv and the thymus lymphomagenic MCF13 murine retroviruses. Deletion mutant analysis revealed that major control regions for MCF13 and Akv LTR enhancer activity were similar but not identical. For both LTRs, major control regions were distinctly different in a murine T-cell and a fibroblast cell line. Recombinant enhancer analysis showed that LTRs could be divided into three regions capable of altering the level of enhancer activity through cooperative or antagonistic interaction. The contribution of each region to enhancer activity was dependent on its context with respect to the other regions. LTR enhancer function in different cell types appears to be the result of the interaction of enhancer modular elements.
我们利用缺失和重组长末端重复序列（LTR）突变体来检测非致病性Akv和胸腺淋巴瘤致瘤性MCF13鼠逆转录病毒的LTR之间的增强子活性差异。缺失突变体分析表明，MCF13和Akv LTR增强子活性的主要控制区域相似但并不相同。对于这两种LTR，在鼠T细胞和成纤维细胞系中，主要控制区域明显不同。重组增强子分析表明，LTR可分为三个区域，这些区域能够通过协同或拮抗相互作用改变增强子活性水平。每个区域对增强子活性的贡献取决于其相对于其他区域的背景。不同细胞类型中LTR增强子功能似乎是增强子模块元件相互作用的结果。
