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首页> 外文期刊>Molecular and Cellular Biology >Transcriptional activation by TFIIB mutants that are severely impaired in interaction with promoter DNA and acidic activation domains.
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Transcriptional activation by TFIIB mutants that are severely impaired in interaction with promoter DNA and acidic activation domains.

机译：TFIIB突变体的转录激活，与启动子DNA和酸性激活域的相互作用受到严重损害。

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Biochemical experiments indicate that the general transcription factor IIB (TFIIB) can interact directly with acidic activation domains and that activators can stimulate transcription by increasing recruitment of TFIIB to promoters. For promoters at which recruitment of TFIIB to promoters is limiting in vivo, one would predict that transcriptional activity should be particularly sensitive to TFIIB mutations that decrease the association of TFIIB with promoter DNA and/or with activation domains; i.e., such TFIIB mutations should exacerbate a limiting step that occurs in wild-type cells. Here, we describe mutations on the DNA-binding surface of TFIIB that severely affect both TATA-binding protein (TBP)-TFIIB-TATA complex formation and interaction with the VP16 activation domain in vitro. These TFIIB mutations affect the stability of the TBP-TFIIB-TATA complex in vivo because they are synthetically lethal in combination with TBP mutants impaired for TFIIB binding. Interestingly, these TFIIB derivatives support viability, and they efficiently respond to Gal4-VP16 and natural acidic activators in different promoter contexts. These results suggest that in vivo, recruitment of TFIIB is not generally a limiting step for acidic activators. However, one TFIIB derivative shows reduced transcription of GAL4, suggesting that TFIIB may be limiting at a subset of promoters in vivo.
机译：生化实验表明，一般转录因子IIB（TFIIB）可以直接与酸性激活域相互作用，并且激活剂可以通过增加TFIIB向启动子的募集来刺激转录。对于在体内限制TFIIB向启动子募集的启动子，人们会预测转录活性对TFIIB突变特别敏感，因为TFIIB突变会降低TFLIB与启动子DNA和/或活化域的结合。即，这种TFIIB突变应加剧在野生型细胞中发生的限制性步骤。在这里，我们描述了TFIIB的DNA结合表面上的突变，该突变会严重影响TATA结合蛋白（TBP）-TFIIB-TATA复合物的形成以及体外与VP16激活域的相互作用。这些TFIIB突变会影响TBP-TFIIB-TATA复合物在体内的稳定性，因为它们与受TFIIB结合影响的TBP突变体联合使用具有致命的杀伤力。有趣的是，这些TFIIB衍生物支持生存能力，并且它们在不同的启动子环境中有效响应Gal4-VP16和天然酸性激活剂。这些结果表明，在体内，TFIIB的募集通常不是酸性活化剂的限制步骤。但是，一种TFIIB衍生物显示GAL4的转录减少，这表明TFIIB可能在体内限制了一部分启动子。

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