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首页> 外文期刊>Molecular and Cellular Biology >Enhancer I Predominance in Hepatitis B Virus Gene Expression
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Enhancer I Predominance in Hepatitis B Virus Gene Expression

机译：乙型肝炎病毒基因表达中的增强子I优势。

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Previous studies of human hepatitis B virus (HBV) transcription revealed the requirement of two enhancer elements. Enhancer I (EnhI) is located upstream of the X promoter and is targeted by multiple activators, including basic leucine zipper proteins, and enhancer II (EnhII) is located upstream to the PreCore promoter and is targeted mainly by nuclear receptors (NRs). The mode of interplay between these enhancers and their unique contributions in regulating HBV transcription remained obscure. By using time course analysis we revealed that the HBV transcripts are categorized into early and late groups. Chang (CCL-13) cells are impaired in expression of the late transcripts. This could be corrected by overexpressing EnhII activators, such as hepatocyte nuclear factor 4α, the retinoid X receptor α, and the peroxisome proliferator-activated receptor α, suggesting that in Chang cells EnhI but not EnhII is active. Replacing the 5′-end EnhI sequence with a synthetic Gal4 response (UAS) DNA fragment ceased the production of the early transcripts. Under this condition NR overexpression poorly activated EnhII. However, activation of the UAS by Gal4-p53 restored both the expression of the early transcripts and the EnhII response to NRs. Thus, a functional EnhI is required for activation of EnhII. We found a major difference between Gal4-p53 and Gal4-VP16 behavior. Gal4-p53 activated the early transcripts, while Gal4-VP16 inhibited the early transcripts but activated the late transcripts. These findings indicate that the composition of the EnhI binding proteins may play a role in early to late switching. Our data provides strong evidence for the role of EnhI in regulating global and temporal HBV gene expression.
机译：先前对人类乙型肝炎病毒（HBV）转录的研究表明需要两种增强子。增强子I（EnhI）位于X启动子的上游，并被包括碱性亮氨酸拉链蛋白在内的多种激活剂靶向，增强子II（EnhII）位于PreCore启动子的上游，主要被核受体（NRs）靶向。这些增强子之间的相互作用模式及其在调节HBV转录中的独特作用仍然不清楚。通过时程分析，我们发现HBV转录本分为早期和晚期组。 Chang（CCL-13）细胞的后期转录表达受损。这可以通过过量表达EnhII激活剂来纠正，例如肝细胞核因子4α，类维生素A X受体α和过氧化物酶体增殖物激活的受体α，这表明在Chang细胞中EnhI而不是EnhII是有活性的。用合成的Gal4响应（UAS）DNA片段代替5'-末端EnhI序列可终止早期转录本的产生。在这种情况下，NR过表达不能充分激活EnhII。但是，Gal4-p53对UAS的激活既恢复了早期转录本的表达，又恢复了EnhII对NR的应答。因此，功能性EnhI是激活EnhII所必需的。我们发现Gal4-p53和Gal4-VP16行为之间的主要区别。 Gal4-p53激活了早期转录本，而Gal4-VP16抑制了早期转录本，但激活了晚期转录本。这些发现表明，EnhI结合蛋白的组成可能在早期到晚期转换中起作用。我们的数据为EnhI在调节整体和暂时性HBV基因表达中的作用提供了有力的证据。

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