Formation of a functional hepatitis B virus replication initiation complex involves a major structural alteration in the RNA template
Formation of a functional hepatitis B virus replication initiation complex involves a major structural alteration in the RNA template
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DOI：
10.1128/mcb.18.11.6265
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发表时间：
1998-11-01
影响因子：
5.3
通讯作者：
Nassal, M
中科院分区：
文献类型：
--
作者：
Beck, J;Nassal, M
乙型肝炎病毒的DNA基因组是由RNA前基因组的逆转录产生的。复制起始不涉及核酸引物；相反，肝病毒P蛋白与结构化RNA封装信号epsilon结合，从中复制一个短的DNA引物，该引物与酶共价连接。利用体外翻译的鸭乙型肝炎病毒（DHBV） P蛋白，研究了该蛋白结合的DHBV epsilon RNA （D epsilon）的二级结构，发现与游离的D epsilon RNA相比，其构象发生了显著变化。一些具有不同自由状态结构的起始能力突变rna也发生了类似的改变，而一个具有结合能力但缺乏起始能力的突变rna则没有发生类似的改变，这表明重排对复制起始的重要性，并提示了与衣壳化的机制耦合。
The DNA genome of a hepatitis B virus is generated by reverse transcription of the RNA pregenome. Replication initiation does not involve a nucleic acid primer; instead, the hepadnavirus P protein binds to the structured RNA encapsidation signal epsilon, from which it copies a short DNA primer that becomes covalently linked to the enzyme. Using in vitro-translated duck hepatitis B virus (DHBV) P protein, we probed the secondary structure of the protein-bound DHBV epsilon RNA (D epsilon) and observed a marked conformational change compared to free D epsilon RNA. Several initiation-competent mutant RNAs with a different free-state structure were similarly altered, whereas a binding-competent but initiation-deficient variant was not, indicating the importance of the rearrangement for replication initiation and suggesting a mechanistic coupling to encapsidation.