Hughes F J, Romanos M A
Department of Cell Biology, Wellcome Research Laboratories, Beckenham, Kent, UK.
Nucleic Acids Res. 1993 Dec 25;21(25):5817-23. doi: 10.1093/nar/21.25.5817.
Replication of human papillomavirus (HPV) DNA requires the viral proteins E1 and E2. Amino acid similarities to SV40 large-T antigen had suggested that E1 is a DNA helicase/ATPase involved in initiating viral DNA replication, and this has recently been shown for bovine papillomavirus type 1 (BPV-1) E1 protein. However, in vitro analysis of HPV E1 has been hampered by the inability to produce purified protein using heterologous expression systems. We have succeeded in demonstrating ATPase and DNA helicase activities in purified HPV E1, expressed in E. coli as a maltose-binding protein fusion (MBP-E1), for the first time. As further confirmation that the ATPase and DNA helicase activities are due to E1 and not contaminating E. coli enzymes, we have shown that a fusion protein containing an amino acid change (E1 Pro-479 to Ser), predicted to inactivate ATP-binding, has impaired activities. We have carried out a structure prediction analysis which suggests that E1 may form two domains: a relatively open N-terminal domain (residues 1-125), and a highly structured C-terminal domain (170-649), with an intermediate region (125-170) predicted to form an inter-domain linker. This is consistent with the proteolytic susceptibility of MBP-E1 at a site 15-20 kD from the N-terminus of E1, and the accumulation of a 58 kD C-terminal fragment of E1. We speculate that the N-terminal domain is involved in DNA-binding, while the C-terminal 58 kD may constitute a distinct enzymatic domain. HPV E1 is of interest as a therapeutic target and the availability of pure enzyme will be invaluable in the search for antiviral compounds.
人乳头瘤病毒(HPV)DNA的复制需要病毒蛋白E1和E2。与猴空泡病毒40(SV40)大T抗原的氨基酸相似性表明,E1是一种参与启动病毒DNA复制的DNA解旋酶/ATP酶,最近在1型牛乳头瘤病毒(BPV-1)E1蛋白中也得到了证实。然而,由于无法使用异源表达系统生产纯化蛋白,HPV E1的体外分析受到了阻碍。我们首次成功地在以麦芽糖结合蛋白融合形式(MBP-E1)在大肠杆菌中表达的纯化HPV E1中证明了ATP酶和DNA解旋酶活性。为了进一步证实ATP酶和DNA解旋酶活性是由E1引起的,而非大肠杆菌酶的污染,我们发现含有一个氨基酸变化(E1第479位脯氨酸变为丝氨酸)的融合蛋白,预计该变化会使ATP结合失活,其活性受损。我们进行了结构预测分析,结果表明E1可能形成两个结构域:一个相对开放的N端结构域(第1至125位氨基酸残基)和一个高度结构化的C端结构域(第170至649位氨基酸残基),中间区域(第125至170位氨基酸残基)预计形成一个结构域间连接区。这与MBP-E1在距离E1 N端15 - 20 kD处的蛋白酶敏感性以及E1的58 kD C端片段的积累情况一致。我们推测N端结构域参与DNA结合,而C端的58 kD可能构成一个独特的酶结构域。HPV E1作为一个治疗靶点备受关注,纯酶的可得性对于寻找抗病毒化合物将具有极高的价值。