Feng W C, Southwood C M, Bieker J J
Department of Physiology, Mount Sinai School of Medicine, New York, New York 10029.
J Biol Chem. 1994 Jan 14;269(2):1493-500.
We describe functional tests and molecular modeling of erythroid Krüppel-like factor (EKLF) interactions with its DNA binding site. EKLF, a zinc finger-containing, erythroid-specific transcription factor, binds and transactivates from the CACCC element, an evolutionarily conserved DNA sequence present within a large number of erythroid-specific promoters and enhancers. This DNA binding element is the site of naturally occurring point mutations that give rise to beta-thalassemia. We have directly tested whether CAC site point mutations (including two of the beta-thalassemia mutants) affect EKLF transactivation and DNA binding function. In vivo analyses demonstrate that EKLF is unable to transactivate a reporter plasmid that contains these mutations. In vitro analyses reveal a 40-100-fold decrease in binding affinity for these sites that accounts for the in vivo observations. The homology between the three EKLF and Zif268 zinc fingers and their conserved sequence-specific contacts to their target site allowed us to formulate a molecular model of the EKLF/CAC site complex, based primarily on energy minimization/refinement of the Zif268/DNA co-crystal structure. These models suggest that both specific and nonspecific hydrogen bonding play a critical role in the ability of EKLF to prefer binding to its cognate site. Analysis of sequence-specific contacts by EKLF to its target site within the beta-globin promoter verified the residues predicted to be important by the functional and modeling data. Together these results demonstrate that EKLF displays a strong discriminatory ability among potential DNA target sites consistent with the beta-thalassemia data. They also suggest that lack of EKLF binding to these sites may play a determining role in its phenotype, and they strengthen the evidence in favor of EKLF's proposed role in erythroid-specific transcriptional activation through the CACCC elements.
我们描述了红系克勒ppel样因子(EKLF)与其DNA结合位点相互作用的功能测试和分子建模。EKLF是一种含锌指的红系特异性转录因子,它能结合并从CACCC元件激活转录,CACCC元件是一种存在于大量红系特异性启动子和增强子中的进化保守DNA序列。这个DNA结合元件是导致β地中海贫血的自然发生点突变的位点。我们直接测试了CAC位点的点突变(包括两个β地中海贫血突变体)是否影响EKLF的转录激活和DNA结合功能。体内分析表明,EKLF无法激活含有这些突变的报告质粒。体外分析显示,对这些位点的结合亲和力下降了40 - 100倍,这解释了体内观察结果。三个EKLF和Zif268锌指之间的同源性以及它们与靶位点保守的序列特异性接触,使我们能够主要基于Zif268/DNA共晶体结构的能量最小化/优化,构建EKLF/CAC位点复合物的分子模型。这些模型表明,特异性和非特异性氢键在EKLF优先结合其同源位点的能力中都起着关键作用。对EKLF与β珠蛋白启动子内靶位点的序列特异性接触分析,验证了功能和建模数据预测的重要残基。这些结果共同表明,EKLF在潜在的DNA靶位点之间表现出很强的鉴别能力,这与β地中海贫血数据一致。它们还表明,EKLF与这些位点缺乏结合可能在其表型中起决定性作用,并且它们加强了支持EKLF通过CACCC元件在红系特异性转录激活中所提出作用的证据。