Mutational analysis of the trans-activation-responsive region of the human immunodeficiency virus type I long terminal repeat
Mutational analysis of the trans-activation-responsive region of the human immunodeficiency virus type I long terminal repeat
复制标题
人类免疫缺陷病毒I型长末端重复序列反式激活反应区的突变分析
作者：
J. Hauber;B. Cullen
我们使用定点诱变技术来描述人类免疫缺陷病毒I型（HIV-I）长末端重复序列（LTR）内的序列，这些序列是病毒基因产物反式激活所必需的。我们证明了序列3'到LTR位置+44对于反式激活是必不可少的，但几乎所有位于位置-17和+44之间的突变在转录和转录后水平上都大大降低了反式激活。然而，通过在LTR TATA盒和cap位点之间插入多达32个碱基对来置换HIV-I LTR反式激活响应区（TAR） 3'，对反式激活几乎没有影响。对转染培养的HIV-I LTR中dna酶I超敏谱的分析表明，至少存在两个dna酶I超敏位点，其中一个延伸到病毒TAR元件；然而，这两个位点似乎都没有受到这种共表达的显著影响。这些结果允许更精确地描述对TAR功能重要的序列，并表明TAR可能被宿主特异性dna结合蛋白识别，而不是直接被该蛋白识别。
We used site-directed mutagenesis to delineate sequences within the human immunodeficiency virus type I (HIV-I) long terminal repeat (LTR) required for trans-activation by the viral tat gene product. We demonstrated that sequences 3' to LTR position +44 are dispensable for trans-activation but that almost all of the mutations tested located between positions -17 and +44 greatly reduced trans-activation at both the transcriptional and posttranscriptional levels. However, displacement of the HIV-I LTR trans-activation-responsive region (TAR) 3' by insertion of up to 32 base pairs between the LTR TATA box and cap site had little effect on trans-activation. An analysis of the DNase I hypersensitivity profile of the HIV-I LTR in transfected cultures suggested the presence of at least two DNase I-hypersensitive sites, including one which extends into the viral TAR element; however, neither of these sites appeared to be significantly affected by tat coexpression. These results allow more precise delineation of the sequences important for TAR function and suggest that the TAR may be recognized by a host-specific DNA-binding protein rather than by the tat protein directly.
与获得性免疫缺陷综合征相关的病毒 3 开放阅读框多态性，人类 T 淋巴细胞病毒 III 型。
影响因子：
14.9
作者：
Ratner,L;Starcich,B;Josephs,SF;Hahn,BH;Reddy,EP;Livak,KJ;PettewayJr,SR;Pearson,ML;Haseltine,WA;Arya,SK
通讯作者：
Arya,SK
影响因子：
11.4
作者：
GARCIA, JA;WU, FK;GAYNOR, RB
通讯作者：
GAYNOR, RB