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首页> 外文期刊>Molecular and Cellular Biology >Simian virus 40 T antigen alters the binding characteristics of specific simian DNA-binding factors.
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Simian virus 40 T antigen alters the binding characteristics of specific simian DNA-binding factors.

机译：猿猴40 T抗原改变了特定猿猴DNA结合因子的结合特性。

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The late promoter of simian virus 40 is transcriptionally activated, in trans, by large T antigen, the primary viral early gene product. Although large T antigen is a well-characterized DNA-binding protein, a variety of data suggest that its trans-activation function does not require direct interaction with DNA. We demonstrate that defined late promoter elements, omega (omega), tau (tau), and delta (delta), necessary for T-antigen-mediated trans-activation, are binding sites for simian cellular factors, not T antigen. Two of the late promoter elements (omega and tau) are shown to bind the same factor or family of factors. These factors bind to a site very similar to that for the HeLa cell factor AP1. We refer to these factors as the simian AP1-sequence recognition proteins (sAP1-SRPs). Compared with normal simian CV-1P cells, the sAP1-SRPs from T-antigen-producing COS cells, or from 14-h simian virus 40-infected CV-1P cells, showed altered binding patterns to both the omega and tau binding sites. In addition, the sAP1-SRPs from T-antigen-containing cells bound to the tau site more stably than did the analogous factors from normal CV-1P cells. The altered pattern of binding and the increased stability of binding correlated with the presence of T antigen in the cell. Additionally, the alteration of the binding pattern within 14 h of infection in CV-1P cells is temporally correct for late promoter activation. Overall, the data show (i) that the late promoter elements necessary for T-antigen-mediated trans-activation contain binding sites for simian cellular DNA-binding proteins; (ii) that the presence of T antigen causes alterations in the binding characteristics of specific simian cellular DNA-binding factors or families of factors; and (iii) that factors which bind to the late promoter elements required for activation have altered and more stable binding characteristics in the presence of T antigen. These points strongly suggest that T antigen mediates trans-activation indirectly through the alteration of binding of at least one specific simian cellular factor, sAP1-SRP, or through the induction of a family of sAP1-SRP factors.
机译：猿猴病毒40的晚期启动子被大T抗原反式转录激活初级病毒早期基因产物。尽管大的T抗原是一个很好表征的DNA结合蛋白，但各种数据表明，其反式激活功能不需要与DNA的直接相互作用。我们证明，T抗原介导的反式激活所必需的已定义的晚期启动子元素，ω（ω），tau（tau）和delta（delta），是猿猴细胞因子而非T抗原的结合位点。已显示晚期启动子元件中的两个（ω和tau）结合相同的因子或因子家族。这些因子与HeLa细胞因子AP1的结合位点非常相似。我们将这些因素称为猿猴AP1序列识别蛋白（sAP1-SRPs）。与正常猿猴CV-1P细胞相比，来自产生T抗原的COS细胞或14-h猿猴病毒40感染的CV-1P细胞的sAP1-SRPs对Ω和tau结合位点的结合方式都有改变。此外，来自含T抗原的细胞的sAP1-SRP与正常CV-1P细胞的类似因子相比，与tau位点的结合更为稳定。结合模式的改变和结合稳定性的提高与细胞中T抗原的存在有关。此外，在CV-1P细胞感染后14小时内，结合模式的改变在时间上对于后期启动子激活是正确的。总体而言，数据表明：（i）T抗原介导的反式激活所必需的晚期启动子元件含有猿猴细胞DNA结合蛋白的结合位点; （ii）T抗原的存在引起特定猿猴细​​胞DNA结合因子或因子家族的结合特性改变; （iii）在存在T抗原的情况下，与激活所需的晚期启动子元件结合的因子已经改变并且更加稳定。这些观点强烈暗示，T抗原通过改变至少一种特定的猿猴细胞因子sAP1-SRP的结合或通过诱导sAP1-SRP因子家族而间接地介导反式激活。

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