De-Medina T, Faktor O, Shaul Y
Department of Virology, Weizmann Institute of Science, Rehovot, Israel.
Mol Cell Biol. 1988 Jun;8(6):2449-55. doi: 10.1128/mcb.8.6.2449-2455.1988.
The S promoter, one of the major hepatitis B virus (HBV) promoters, directs the synthesis of mRNA for surface antigen. Transient expression studies revealed that this promoter is highly active in the Alexander hepatoma cell line but not in SK-Hep1 and HeLa cells. We found that a distal element of the promoter (-103 to -48) confers this cell-type-specific behavior through a mechanism in which the promoter activity is repressed in HeLa and SK-Hep1 cells but increased in Alexander cells. By using an inhibitor of protein synthesis, we obtained evidence that a labile repressor(s) confers the negative effect in SK-Hep1 cells. We also found an enhancerlike activity associated with a small DNA segment of the S promoter (-27 to + 30). This proximal element was active in HeLa and SK-Hep1 cells only in the absence of the distal negative element. Finally, analysis of S promoter deletion mutants demonstrated that the -27 to -17 region of the S promoter is crucial for its activity.
S启动子是乙型肝炎病毒（HBV）的主要启动子之一，指导表面抗原mRNA的合成。瞬时表达研究表明，该启动子在亚历山大肝癌细胞系中高度活跃，但在SK-Hep1和HeLa细胞中不活跃。我们发现，启动子的一个远端元件（-103至-48）通过一种机制赋予这种细胞类型特异性行为，即启动子活性在HeLa和SK-Hep1细胞中受到抑制，但在亚历山大细胞中增加。通过使用蛋白质合成抑制剂，我们获得证据表明，一种不稳定的阻遏物在SK-Hep1细胞中产生负面影响。我们还发现与S启动子的一个小DNA片段（-27至+30）相关的增强子样活性。该近端元件仅在没有远端负元件的情况下在HeLa和SK-Hep1细胞中具有活性。最后，对S启动子缺失突变体的分析表明，S启动子的-27至-17区域对其活性至关重要。
