Kawaguchi Y, Maeda K, Ono M, Yokoyama N, Tsubota K, Fujita K, Tohya Y, Kai C, Mikami T
Department of Veterinary Microbiology, Faculty of Agriculture, University of Tokyo, Japan.
J Vet Med Sci. 1996 Aug;58(8):715-21. doi: 10.1292/jvms.58.715.
We analyzed the mechanism for feline herpesvirus type 1 (FHV-1) immediate early (IE) gene expression. We demonstrated that (i) the transcription initiation site of the FHV-1 IE transcript lies in the putative FHV-1 ICP4 binding site, (ii) the FHV-1 IE transcript is spliced to remove 906 bp intron from the leader region, (iii) cis-acting elements of the FHV-1 IE promoter map both down- and upstream of the transcription initiation site, and (iv) a deletion of a 58 bp sequence which includes the putative FHV-1 ICP4 binding site in the IE promoter resulted in significant induction of promoter activity by a FHV-1 IE gene product although the FHV-1 IE gene product slightly stimulates the FHV-1 IE promoter, indicating that the FHV-1 IE gene product down-regulates its own promoter via the region.
我们分析了猫疱疹病毒1型(FHV-1)立即早期(IE)基因表达的机制。我们证明:(i)FHV-1 IE转录本的转录起始位点位于假定的FHV-1 ICP4结合位点;(ii)FHV-1 IE转录本经过剪接,从先导区去除了906 bp的内含子;(iii)FHV-1 IE启动子的顺式作用元件定位于转录起始位点的下游和上游;(iv)IE启动子中一个包含假定的FHV-1 ICP4结合位点的58 bp序列的缺失,导致FHV-1 IE基因产物对启动子活性有显著诱导作用,尽管FHV-1 IE基因产物对FHV-1 IE启动子有轻微刺激,这表明FHV-1 IE基因产物通过该区域下调其自身启动子。