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异质性核糖核蛋白G可阻止剪接位点SA3358和SD3632之间的中央外显子包含在人乳头瘤病毒16型L1信使核糖核酸中。

hnRNP G prevents inclusion on the HPV16 L1 mRNAs of the central exon between splice sites SA3358 and SD3632.

作者信息

Yu Haoran, Gong Lijing, Wu Chengjun, Nilsson Kersti, Li-Wang Xiaoze, Schwartz Stefan

机构信息

Department of Laboratory Medicine, Lund university, BMC-B13, 223 62 Lund, Sweden.

China Academy of Sport and Health Sciences, Beijing Sport University, Xinxi Road 48, Haidian District, 100084 Beijing, PR China.

出版信息

J Gen Virol. 2018 Mar;99(3):328-343. doi: 10.1099/jgv.0.001019.

Abstract

HPV16 late L1 mRNAs encode a short central exon that is located between HPV16 3'-splice site SA3358 and HPV16 5'-splice site SD3632. While SA3358 is used to produce both HPV16 early mRNAs encoding the E6 and E7 oncogenes, and late mRNAs encoding E4, L1 and L2, SD3632 is used exclusively to produce late L1 mRNA. We have previously identified an 8-nucleotide regulatory RNA element that is required for inclusion of the exon between SA3358 and SD3632 to produce L1 mRNAs at the expense of mRNAs polyadenylated at the HPV16 early polyadenylation signal pAE. Here we show that this HPV16 8-nucleotide splicing enhancer interacts with hnRNP G. Binding of hnRNP G to this element prevents inclusion of the exon between SA3358 and SD3632 on the HPV16 late L1 mRNAs. We concluded that hnRNP G has a splicing inhibitory role and that hnRNP G can control HPV16 mRNA splicing.

摘要

人乳头瘤病毒16型(HPV16)晚期L1信使核糖核酸(mRNAs)编码一个短的中央外显子,该外显子位于HPV16 3'-剪接位点SA3358和HPV16 5'-剪接位点SD3632之间。虽然SA3358用于产生编码E6和E7致癌基因的HPV16早期mRNAs以及编码E4、L1和L2的晚期mRNAs,但SD3632仅用于产生晚期L1 mRNA。我们之前鉴定出一种8个核苷酸的调节性RNA元件,该元件是将SA3358和SD3632之间的外显子纳入以产生L1 mRNAs所必需的,而以在HPV16早期多聚腺苷酸化信号pAE处多聚腺苷酸化的mRNAs为代价。在此我们表明,这种HPV16 8个核苷酸的剪接增强子与不均一核糖核蛋白G(hnRNP G)相互作用。hnRNP G与该元件的结合会阻止SA3358和SD3632之间的外显子纳入HPV16晚期L1 mRNAs。我们得出结论,hnRNP G具有剪接抑制作用,并且hnRNP G可以控制HPV16 mRNA剪接。

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