Bouallaga I, Massicard S, Yaniv M, Thierry F
Département des biotechnologies, URA 1644 du CNRS, Institut Pasteur, Paris, France.
EMBO Rep. 2000 Nov;1(5):422-7. doi: 10.1093/embo-reports/kvd091.
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, HPV18 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).
最近的研究报道了介导强组织特异性增强子转录协同作用的新机制，这些机制涉及称为增强体的高阶核蛋白复合物的协同组装。在这里，我们表明，控制E6和E7转化基因上皮特异性转录的HPV18增强子具有这些结构的特征。我们通过缺失实验表明，一个核心增强子元件以特定的螺旋相位与结合在增强子末端的远距离必需因子协同作用。这个结合Jun B/Fra-2异二聚体的核心序列在核蛋白复合物中协同招募结构蛋白HMG-I(Y)，在该复合物中它们相互作用。因此，在HeLa细胞中，HPV18转录似乎依赖于一个增强体的组装，该增强体包含由与AP1和HMG-I(Y)相互作用的核心序列招募的多种细胞因子。
