Wache Susanne C, Hoagland Erica M, Zeigler Georgia, Swanson Hollie I
Department of Molecular and Biomedical Pharmacology, University of Kentucky Medical Center, Lexington, KY 40536, USA.
Gene Expr. 2005;12(4-6):231-43. doi: 10.3727/000000005783991981.
The aryl hydrocarbon receptor (AHR) and its DNA binding partner, the aryl hydrocarbon receptor nuclear translocator (ARNT) are basic helix-loop-helix/PAS proteins. The goal of the current study was to determine the extent to which residues R14 and R15 contained within the basic region of the AHR contribute to the DNA binding affinity and stability of the AHR/ARNT heterodimer. Towards this end, we first performed equilibrium binding and dissociation rate analyses using a single dioxin response element (DRE-1). While the K(D) and Bmax values obtained from the equilibrium binding analysis were similar for the wild-type AHR (wt AHR) and that containing the substitutions of R14 and R15 with Q residues (Q14Q15 AHR), dissociation rate analyses revealed that the stability of the Q14Q15 AHR DNA binding complex was approximately 10-fold less. Using a two-site DNA binding model, we also found that AHR/ARNT heterodimer does not participate in cooperative binding, as binding of the second dimer appears to be prohibited by occupation of the first. This property was similar regardless of the composition of the amino acids at positions 14 and 15. Finally, reporter assays revealed that the Q14Q15 substitutions severely compromised the ability of the AHR to activate gene expression despite appropriate nuclear localization. The present results revealed that DNA binding stability of the AHR/ARNT heterodimer is an important requirement for its transactivation capabilities and that this stability is governed, in part, by residues R14 and R15 that lie within the basic region of the AHR.
芳基烃受体(AHR)及其DNA结合伴侣芳基烃受体核转运蛋白(ARNT)是碱性螺旋-环-螺旋/PAS蛋白。本研究的目的是确定AHR碱性区域内的R14和R15残基对AHR/ARNT异二聚体的DNA结合亲和力和稳定性的贡献程度。为此,我们首先使用单个二噁英反应元件(DRE-1)进行了平衡结合和解离速率分析。虽然从平衡结合分析中获得的野生型AHR(wt AHR)和包含用Q残基取代R14和R15的AHR(Q14Q15 AHR)的K(D)和Bmax值相似,但解离速率分析表明,Q14Q15 AHR DNA结合复合物的稳定性约低10倍。使用双位点DNA结合模型,我们还发现AHR/ARNT异二聚体不参与协同结合,因为第二个二聚体的结合似乎被第一个二聚体的占据所阻止。无论第14和15位氨基酸的组成如何,该特性都是相似的。最后,报告基因分析表明,尽管核定位合适,但Q14Q15取代严重损害了AHR激活基因表达的能力。目前的结果表明,AHR/ARNT异二聚体的DNA结合稳定性是其反式激活能力的重要要求,并且这种稳定性部分受位于AHR碱性区域内的R14和R15残基的控制。