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人乳头瘤病毒16型长控制区的染色质结构可抑制病毒癌蛋白的表达。

The chromatin structure of the long control region of human papillomavirus type 16 represses viral oncoprotein expression.

作者信息

Stünkel W, Bernard H U

机构信息

Institute of Molecular and Cell Biology, National University of Singapore, Republic of Singapore.

出版信息

J Virol. 1999 Mar;73(3):1918-30. doi: 10.1128/JVI.73.3.1918-1930.1999.

Abstract

The long control region (LCR) of human papillomavirus type 16 (HPV-16) has a size of 850 bp (about 12% of the viral genome) and regulates transcription and replication of the viral DNA. The 5' segment of the LCR contains transcription termination signals and a nuclear matrix attachment region, the central segment contains an epithelial cell-specific enhancer, and the 3' segment contains the replication origin and the E6 promoter. Here we report observations on the chromatin organization of this part of the HPV-16 genome. Treatment of the nuclei of CaSki cells, a cell line with 500 intrachromosomal copies of HPV-16, with methidiumpropyl-EDTA-Fe(II) reveals nucleosomes in specific positions on the LCR and the E6 and E7 genes. One of these nucleosomes, which we termed Ne, overlaps with the center of the viral enhancer, while a second nucleosome, Np16, overlaps with the replication origin and the E6 promoter. The two nucleosomes become positioned on exactly the same segments after in vitro assembly of chromatin on the cloned HPV-16 LCR. Primer extension mapping of DNase I-cleaved chromatin revealed Np16 to be positioned centrally over E6 promoter elements, extending into the replication origin. Ne covers the center of the enhancer but leaves an AP-1 site, one of the strongest cis-responsive elements of the enhancer, unprotected. Np16, or a combination of Np16 and Ne, represses the activity of the E6 promoter during in vitro transcription of HPV-16 chromatin. Repression is relieved by addition of Sp1 and AP-1 transcription factors. Sp1 alters the structure of Np16 in vitro, while no changes can be observed during the binding of AP-1. HPV-18, which has a similar arrangement of cis-responsive elements despite its evolutionary divergence from HPV-16, shows specific assembly in vitro of a nucleosome, Np18, over the E1 binding site and E6 promoter elements but positioned about 90 bp 5' of the position of Np16 on the homologous HPV-16 sequences. The chromatin organization of the HPV-16 and HPV-18 genomes suggests important regulatory roles of nucleosomes during the viral life cycle.

摘要

人乳头瘤病毒16型(HPV - 16)的长控制区(LCR)大小为850碱基对(约占病毒基因组的12%),可调节病毒DNA的转录和复制。LCR的5'段包含转录终止信号和一个核基质附着区,中间段包含一个上皮细胞特异性增强子,3'段包含复制起点和E6启动子。在此,我们报告了关于HPV - 16基因组这一部分染色质组织的观察结果。用甲哌鎓丙基 - EDTA - Fe(II)处理CaSki细胞(一种含有500个HPV - 16染色体内拷贝的细胞系)的细胞核,可揭示LCR以及E6和E7基因上特定位置的核小体。其中一个核小体,我们称之为Ne,与病毒增强子的中心重叠,而另一个核小体Np16与复制起点和E6启动子重叠。在克隆的HPV - 16 LCR上进行染色质体外组装后,这两个核小体定位在完全相同的片段上。对DNA酶I切割的染色质进行引物延伸图谱分析表明,Np16位于E6启动子元件的中心位置,延伸至复制起点。Ne覆盖增强子的中心,但留下一个AP - 1位点(增强子最强的顺式反应元件之一)未被保护。在HPV - 16染色质的体外转录过程中,Np16或Np16与Ne的组合会抑制E6启动子的活性。通过添加Sp1和AP - 1转录因子可解除抑制。Sp1在体外改变Np16的结构,而在AP - 1结合过程中未观察到变化。HPV - 18尽管与HPV - 16在进化上存在差异,但其顺式反应元件的排列方式相似,在E1结合位点和E6启动子元件上显示出核小体Np18在体外的特异性组装,但其位置在同源HPV - 16序列上比Np16的位置5'端大约90碱基对处。HPV - 16和HPV - 18基因组的染色质组织表明核小体在病毒生命周期中具有重要的调节作用。

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