Qian Z, Brunovskis P, Lee L, Vogt P K, Kung H J
Department of Molecular Biology and Microbiology, School of Medicine, Case Western Reserve University, Cleveland, Ohio 44106, USA.
J Virol. 1996 Oct;70(10):7161-70. doi: 10.1128/JVI.70.10.7161-7170.1996.
Marek's disease virus is a highly oncogenic herpesvirus that can cause T lymphomas and peripheral nerve demyelination in chickens. meq, a candidate oncogene of Marek's disease virus, encodes a basic leucine zipper (bZIP) transcription factor which contains a large proline-rich domain in its C terminus. On the basis of its bZIP structural homology, meq is perhaps the only member of the jun-fos gene family completely viral in origin. We previously showed that Meq's C-terminal domain has potent transactivation activity and that its bZIP domain can dimerize with itself and with c-Jun also. In an effort to identify viral and cellular targets of Meq, we have determined the optimal binding sites for Meq-Jun heterodimers and Meq-Meq homodimers. By a PCR-based approach using cyclic amplification of selected targets, Meq-Jun heterodimers were found to optimally bind tetradecanoylphorbol acetate response element (TRE) and cyclic AMP response element (CRE) consensus sequences. This result was consistent with the results of our previous functional analysis implicating Meq-Jun heterodimers in the transactivation of the Meq promoter through a TRE- or CRE-like sequence. Interestingly, Meq-Meq homodimers were found to bind two distinct motif elements. The first [GAGTGATG AC(G)TCATC] has a consensus which includes a TRE or CRE core flanked by additional nucleotides critical for tight binding. Methylation interference and mutational analyses confirmed the importance of the flanking residues. The sequences of a subset of TRE and CRE sites selected by Meq-Meq are closely related to the binding motif of Maf, another bZIP oncoprotein. The second putative Meq binding site (RACACACAY) bears a completely different consensus not shared by other bZIP proteins. Binding to this consensus sequence also requires secondary structure characteristics associated with DNA bending. CACA motifs are known to promote DNA curvature and function in a number of special biological processes. Our results lend further weight to the increasing importance of DNA bending in transcriptional regulation and provide a baseline for the identification of Meq-responsive targets.
马立克氏病病毒是一种高度致癌的疱疹病毒,可在鸡体内引发T淋巴瘤和外周神经脱髓鞘。meq是马立克氏病病毒的一个候选致癌基因,编码一种碱性亮氨酸拉链(bZIP)转录因子,其C末端含有一个富含脯氨酸的大结构域。基于其bZIP结构同源性,meq可能是起源完全为病毒的Jun-Fos基因家族的唯一成员。我们之前表明,Meq的C末端结构域具有强大的反式激活活性,并且其bZIP结构域也能与自身以及c-Jun形成二聚体。为了确定Meq的病毒和细胞靶点,我们已经确定了Meq-Jun异源二聚体和Meq-Meq同源二聚体的最佳结合位点。通过基于PCR的方法,利用选定靶点的循环扩增,发现Meq-Jun异源二聚体与十四酰佛波醇乙酸酯反应元件(TRE)和环磷酸腺苷反应元件(CRE)共有序列具有最佳结合。这一结果与我们之前的功能分析结果一致,即Meq-Jun异源二聚体通过类似TRE或CRE的序列参与Meq启动子的反式激活。有趣的是,发现Meq-Meq同源二聚体结合两个不同的基序元件。第一个[GAGTGATG AC(G)TCATC]具有一个共有序列,其中包括一个TRE或CRE核心,两侧是对紧密结合至关重要的额外核苷酸。甲基化干扰和突变分析证实了侧翼残基的重要性。由Meq-Meq选择的一部分TRE和CRE位点的序列与另一种bZIP癌蛋白Maf的结合基序密切相关。第二个假定的Meq结合位点(RACACACAY)具有一个完全不同的共有序列,其他bZIP蛋白不具有该序列。与该共有序列的结合还需要与DNA弯曲相关的二级结构特征。已知CACA基序可促进DNA弯曲并在许多特殊生物学过程中发挥作用。我们的结果进一步证明了DNA弯曲在转录调控中的重要性日益增加,并为鉴定Meq反应靶点提供了一个基线。