Sarid R, Gazit A, Tronick S R, Yaniv A
Department of Human Microbiology, Sackler School of Medicine, Tel-Aviv University, Israel.
Virology. 1995 Apr 20;208(2):789-94. doi: 10.1006/viro.1995.1213.
We analyzed the long terminal repeat (LTR) of the lymphoproliferative disease virus of turkeys for sequences that influence its promoter activity by using the chloramphenicol acetyltransferase assay. A series of LTR deletion mutants and recombinants between LTR and simian virus 40 regulatory sequences were used for these studies. Through transfection experiments, we identified a negative regulatory element residing at the 5' end of the U3. The two imperfect direct repeats (DRs) located at nt - 170 to - 125 upstream of the RNA transcription site were identified as enhancer elements which could stimulate transcription of a heterologous promoter in an orientation independent manner. Specific interaction of nuclear factors with the DRs element was identified. The two DRs contain cArg motifs which are suggested to play a role in tissue specific expression of several cellular genes.
我们通过氯霉素乙酰转移酶测定法,分析了火鸡淋巴细胞增生性疾病病毒的长末端重复序列(LTR)中影响其启动子活性的序列。一系列LTR缺失突变体以及LTR与猿猴病毒40调控序列之间的重组体被用于这些研究。通过转染实验,我们在U3的5'端鉴定出一个负调控元件。位于RNA转录位点上游核苷酸-170至-125处的两个不完全同向重复序列(DRs)被鉴定为增强子元件,它们能够以方向独立的方式刺激异源启动子的转录。我们还鉴定出了核因子与DRs元件的特异性相互作用。这两个DRs包含cArg基序,提示其在几种细胞基因的组织特异性表达中发挥作用。