Erlwein O, Rethwilm A
Institut für Virologie und Immunbiologie der Universität, Würzburg, Germany.
Virology. 1993 Sep;196(1):256-68. doi: 10.1006/viro.1993.1474.
Cis-regulatory elements in the long terminal repeat (LTR) of human foamy virus (HFV) were identified by using LTR mutants to transiently express the chloramphenicol acetyl-transferase gene after co-transfection with an expression plasmid for the virus bel-1 (transactivator) gene. The R-U5 region and an element in the 5' U3 region were found to negatively influence HFV gene expression. The complete BEL-1 responsive region was mapped to extend from nucleotide position -471 to position -93 relative to the start of transcription. Within this region, three elements were identified that in the homologous or a heterologous (SV40) promoter context can, independently and irrespective of their orientation, act as targets for BEL-1. These elements are located between nucleotide positions -413/-378, -361/-291, and -124/93. The target elements do not share obvious sequence homologies. The mechanism of HFV transactivation appears to be novel among the complex retroviruses and is likely to involve, as yet, undiscovered cellular DNA binding factors.
通过使用长末端重复序列（LTR）突变体，在与病毒bel-1（反式激活因子）基因的表达质粒共转染后瞬时表达氯霉素乙酰转移酶基因，从而鉴定了人泡沫病毒（HFV）长末端重复序列（LTR）中的顺式调控元件。发现R-U5区域和5'U3区域中的一个元件对HFV基因表达有负面影响。完整的BEL-1反应区域被定位为从相对于转录起始点的核苷酸位置-471延伸至位置-93。在该区域内，鉴定出三个元件，在同源或异源（SV40）启动子背景下，它们可以独立且不考虑其方向，作为BEL-1的靶标。这些元件位于核苷酸位置-413 / -378、-361 / -291和-124 / 93之间。靶标元件不具有明显的序列同源性。在复杂的逆转录病毒中，HFV反式激活的机制似乎是新颖的，并且可能涉及尚未发现的细胞DNA结合因子。
