Smits P H, Smits H L, Minnaar R P, ter Schegget J
Department of Medical Microbiology, University of Amsterdam, The Netherlands.
J Gen Virol. 1993 Jan;74 ( Pt 1):121-4. doi: 10.1099/0022-1317-74-1-121.
The human papillomavirus type 16 (HPV-16) enhancer-promoter is virtually inactive in normal human diploid fibroblasts, but active in human fibroblasts with a deletion in the short arm of one chromosome 11 (del-11 cells). Since the HPV-16 enhancer with the simian virus 40 promoter is active in both cell types, the target for chromosome 11-regulated HPV-expression is likely to be located in the HPV-16 early promoter region (nucleotides 57 to 112). We show here that DNA-protein complexes formed with an HPV-16 promoter fragment are quantitatively different in del-11 cell and diploid cell extracts. This quantitative difference detected in band shift experiments disappeared upon mutation of the HPV-16 TATAAAA box to TATTTAT. This mutation also strongly reduced the activity of the HPV-16 enhancer-promoter in del-11 cells. These results indicate that TATA-binding proteins are involved in the chromosome 11-mediated regulation of HPV-16 gene expression.
人乳头瘤病毒16型(HPV - 16)增强子 - 启动子在正常人二倍体成纤维细胞中实际上是无活性的,但在11号染色体短臂有缺失的人成纤维细胞(del - 11细胞)中是有活性的。由于带有猿猴病毒40启动子的HPV - 16增强子在这两种细胞类型中都是有活性的,所以11号染色体调控HPV表达的靶点可能位于HPV - 16早期启动子区域(核苷酸57至112)。我们在此表明,与HPV - 16启动子片段形成的DNA - 蛋白质复合物在del - 11细胞提取物和二倍体细胞提取物中在数量上是不同的。在凝胶迁移实验中检测到的这种数量差异在HPV - 16 TATAAAA框突变为TATTTAT后消失。这种突变也强烈降低了HPV - 16增强子 - 启动子在del - 11细胞中的活性。这些结果表明,TATA结合蛋白参与了11号染色体介导的HPV - 16基因表达调控。