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首页> 外文期刊>Molecular and Cellular Biology >DNA-binding properties of simian virus 40 T-antigen mutants defective in viral DNA replication.
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DNA-binding properties of simian virus 40 T-antigen mutants defective in viral DNA replication.

机译：猿猴病毒40 T抗原突变体的DNA结合特性在病毒DNA复制中存在缺陷。

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Three simian virus 40 (SV40)-transformed monkey cell lines, C2, C6, and C11, producing T-antigen variants that are unable to initiate viral DNA replication, were analyzed with respect to their affinity for regulatory sequences at the viral origin of replication. C2 and C11 T antigens both bound specifically to sequences at sites 1 and 2 at the viral origin region, whereas C6 T antigen showed no specific affinity for any viral DNA sequences under all conditions tested. Viral DNA sequences encoding the C6 T antigen have recently been cloned out of C6 cells and used to transform an established rat cell line. T antigen from several cloned C6-SV40-transformed rat lines failed to bind specifically to the origin. C6 DNA contains three mutations: two located close to the amino terminus of T antigen at amino acid positions 30 and 51 and a third located internally at amino acid position 153. Two recombinant SV40 DNA mutants were prepared containing either the amino-terminal mutations at positions 30 and 51 (C6-1) or the internally located mutation at position 153 (C6-2) and used to transform Rat 2 cells. Whereas T antigen from C6-2-transformed cells lacked any specific affinity for these sequences. Therefore, the single mutation at amino acid position 153 (Asn leads to Thr) is sufficient to abolish the origin-binding property of T antigen. A T antigen-specific monoclonal antibody, PAb 100, which had been previously shown to immunoprecipitate an immunologically distinct origin-binding subclass of T antigen, recognized wild-type or C6-1 antigens, but failed to react with C6 or C6-2 T antigens. These results indicate that viral replication function comprises properties of T antigen that exist in addition to its ability to bind specifically to the SV40 regulatory sequences. Furthermore, it is concluded from these data that specific viral origin binding is not a necessary feature of the transforming function of T antigen.
机译：分析了三种猿猴病毒40（SV40）转化的猴细胞系C2，C6和C11，它们产生了无法启动病毒DNA复制的T抗原变异体，它们对病毒复制起点上的调控序列的亲和力。 C2和C11 T抗原都与病毒起源区域第1位和第2位的序列特异性结合，而C6 T抗原在所有测试条件下对任何病毒DNA序列均无特异性亲和力。最近已从C6细胞中克隆出编码C6 T抗原的病毒DNA序列，并用于转化已建立的大鼠细胞系。来自几个克隆的经C6-SV40转化的大鼠品系的T抗原不能特异性地与来源结合。 C6 DNA包含三个突变：两个位于T抗原氨基末端附近的第30和51位氨基酸，第三个内部位于T氨基酸的第153位氨基酸。制备了两个重组SV40 DNA突变体，在其中的两个氨基酸末端均含有突变30和51（C6-1）或位于153位的内部突变（C6-2），并用于转化Rat 2细胞。而来自C6-2-转化细胞的T抗原对这些序列缺乏任何特异性亲和力。因此，在氨基酸位置153的单一突变（Asn导致Thr）足以消除T抗原的起源结合特性。 AT抗原特异性单克隆抗体PAb 100，先前已显示能免疫沉淀T抗原的免疫学上独特的起源结合亚类，可以识别野生型或C6-1抗原，但无法与C6或C6-2 T抗原反应。这些结果表明，病毒复制功能除了具有与SV40调控序列特异性结合的能力外，还包括T抗原的存在。此外，从这些数据可以得出结论，特定的病毒起源结合不是T抗原转化功能的必要特征。

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