An enhanceosome containing the Jun B/Fra-2 heterodimer and the HMG-I(Y) architectural protein controls HPV18 transcription
An enhanceosome containing the Jun B/Fra-2 heterodimer and the HMG-I(Y) architectural protein controls HPV18 transcription
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DOI：
10.1093/embo-reports/kvd091
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发表时间：
2000-11-01
期刊：
影响因子：
7.7
通讯作者：
Thierry, F
中科院分区：
文献类型：
--
作者：
Bouallaga, I;Massicard, S;Thierry, F
最近的研究报道了介导强组织特异性增强子的转录协同作用的新机制，涉及称为增强体的高阶核蛋白复合物的合作组装。在这里，我们表明，HPV 18增强子，控制上皮特异性转录的E6和E7转化基因，表现出这些结构的特征。我们用删除实验表明，核心增强子元件合作，在一个特定的螺旋定相，与遥远的必需因子结合的增强子的末端。该核心序列结合Jun B/Fra-2异二聚体，协同募集核蛋白复合物中的结构蛋白HMG-I（Y），在那里它们彼此相互作用。因此，在HeLa细胞中，HPV 78的转录似乎依赖于增强体的组装，增强体包含由与AP 1和HMG-I（Y）相互作用的核心序列募集的多种细胞因子。
Recent studies have reported new mechanisms that mediate the transcriptional synergy of strong tissue-specific enhancers, involving the cooperative assembly of higher-order nucleoprotein complexes called enhanceosomes. Here we show that the HPV18 enhancer, which controls the epithelial-specific transcription of the E6 and E7 transforming genes, exhibits characteristic features of these structures. We used deletion experiments to show that a core enhancer element cooperates, in a specific helical phasing, with distant essential factors binding to the ends of the enhancer. This core sequence, binding a Jun B/Fra-2 heterodimer, cooperatively recruits the architectural protein HMG-I(Y) in a nucleoprotein complex, where they interact with each other. Therefore, in HeLa cells, HPV78 transcription seems to depend upon the assembly of an enhanceosome containing multiple cellular factors recruited by a core sequence interacting with AP1 and HMG-I(Y).