Williams J L, Cann A J, Leff T, Sassone-Corsi P, Chen I S
Department of Medicine, UCLA School of Medicine.
Nucleic Acids Res. 1989 Jul 25;17(14):5737-49. doi: 10.1093/nar/17.14.5737.
The tax protein of HTLV-II increases the level of steady-state mRNA produced from the HTLV-II long terminal repeat (LTR) and also activates heterologous promoters. We have previously shown that the adenovirus E3 promoter, which is trans-activated by the adenovirus E1a protein, is also trans-activated by the tax protein. To investigate the mechanism of trans-activation by tax, we analyzed E3 promoter deletion mutants to determine nucleotide sequence requirements for activation of this promoter. Our results show that removal of different upstream regions within the promoter does not result in loss of trans-activation, indicating that tax does not appear to interact with a single DNA binding protein to activate the E3 promoter. In addition, tax and E1a together activate the E3 promoter in a greater than additive fashion, suggesting that these proteins function differently. Possible mechanisms of activation by the tax protein are discussed.
人类嗜T淋巴细胞病毒II型(HTLV-II)的tax蛋白可提高由HTLV-II长末端重复序列(LTR)产生的稳态mRNA水平,还能激活异源启动子。我们之前已经表明,腺病毒E3启动子,可被腺病毒E1a蛋白反式激活,也能被tax蛋白反式激活。为了研究tax反式激活的机制,我们分析了E3启动子缺失突变体,以确定激活该启动子所需的核苷酸序列。我们的结果表明,去除启动子内不同的上游区域不会导致反式激活作用的丧失,这表明tax似乎不会与单一的DNA结合蛋白相互作用来激活E3启动子。此外,tax和E1a共同以大于相加的方式激活E3启动子,这表明这些蛋白的功能有所不同。文中讨论了tax蛋白激活的可能机制。