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人类1型T细胞白血病病毒PR76(gag-pro)转框蛋白中的一个新型蛋白酶切割位点确定了逆转录酶的N端。

A novel protease processing site in the transframe protein of human T-cell leukemia virus type 1 PR76(gag-pro) defines the N terminus of RT.

作者信息

Heidecker Gisela, Hill Shawn, Lloyd Patricia A, Derse David

机构信息

Basic Research Laboratory, NCI-Frederick, Building 567, Room 154, Frederick, MD 21702-1201, USA.

出版信息

J Virol. 2002 Dec;76(24):13101-5. doi: 10.1128/jvi.76.24.13101-13105.2002.

Abstract

The genomic RNA of human T-cell leukemia virus type 1 encodes three polyproteins, Gag, Gag-Pro, and Gag-Pro-Pol, which are translated as a result of no, one, and two frameshifts, respectively. In this report we demonstrate that the 77 residues encoded at the C terminus of the Gag-Pro precursor can be collectively detected as an 8-kDa transframe protein (TFP) in virions. Mutant viruses with a C-terminally truncated TFP (19, 32, or 50 residues) had essentially a wild-type phenotype in vitro. However, a virus mutant that encoded only the Gag and Gag-Pro-Pol polyproteins due to a mutation in the second frameshift site, and hence did not produce TFP, was noninfectious. Mutation analysis of the proteolytic cleavage site between PR and TFP revealed the presence of an additional site and the existence of a p1 peptide separating protease and TFP. While removal of the cleavage site at the PR-p1 junction had a modest effect on virus replication, mutation of the p1-TFP cleavage site led to noninfectious virus and the loss of reverse transcriptase activity. Determination of the amino-terminal sequence of a hemagglutinin-tagged RT demonstrated that the same site is used in processing the Gag-Pro-Pol precursor and thus defines the start of mature RT. Neither mutation alone or in combination caused changes in the amounts or processing patterns of the Gag polyprotein, indicating that protease is active independent of its C terminus.

摘要

1型人类T细胞白血病病毒的基因组RNA编码三种多聚蛋白,即Gag、Gag-Pro和Gag-Pro-Pol,它们分别通过零次、一次和两次移码翻译产生。在本报告中,我们证明在病毒颗粒中,可以共同检测到Gag-Pro前体C末端编码的77个残基作为一种8 kDa的移码蛋白(TFP)。C末端截短的TFP(19、32或50个残基)的突变病毒在体外基本上具有野生型表型。然而,由于第二个移码位点发生突变而仅编码Gag和Gag-Pro-Pol多聚蛋白,因此不产生TFP的病毒突变体无感染性。对蛋白酶(PR)和TFP之间的蛋白水解切割位点进行突变分析,发现存在一个额外的位点以及一个分隔蛋白酶和TFP的p1肽。虽然去除PR-p1连接处的切割位点对病毒复制有适度影响,但p1-TFP切割位点的突变导致无感染性病毒并丧失逆转录酶活性。对血凝素标记的逆转录酶(RT)的氨基末端序列进行测定表明,在加工Gag-Pro-Pol前体时使用了相同的位点,因此确定了成熟RT的起始位置。单独或组合的突变均未引起Gag多聚蛋白的量或加工模式的变化,表明蛋白酶的活性与其C末端无关。

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