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人巨细胞病毒 RNA2.7 通过减少 RNA 聚合酶 II（Pol II）与磷酸化细胞周期蛋白依赖性激酶 9（pCDK9）之间的相互作用，抑制 Pol II 丝氨酸-2 的磷酸化。

Human cytomegalovirus RNA2.7 inhibits RNA polymerase II (Pol II) Serine-2 phosphorylation by reducing the interaction between Pol II and phosphorylated cyclin-dependent kinase 9 (pCDK9).

机构信息

Virology Laboratory, Shengjing Hospital of China Medical University, Shenyang, 110004, China; Department of Pediatrics, Shengjing Hospital of China Medical University, Shenyang, 110004, China; Department of Obstetrics and Gynecology, Shengjing Hospital of China Medical University, Shenyang, 110004, China.

Department of Pediatrics, The Fourth Affiliated Hospital, China Medical University, Shenyang, 110033, China.

出版信息

Virol Sin. 2022 Jun;37(3):358-369. doi: 10.1016/j.virs.2022.02.011. Epub 2022 Feb 28.

DOI:10.1016/j.virs.2022.02.011
PMID:35537980
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9243627/
Abstract

Human cytomegalovirus (HCMV) is a ubiquitous pathogen belongs to betaherpesvirus subfamily. RNA2.7 is a highly conserved long non-coding RNA accounting for more than 20% of total viral transcripts. In our study, functions of HCMV RNA2.7 were investigated by comparison of host cellular transcriptomes between cells infected with HCMV clinical strain and RNA2.7 deleted mutant. It was demonstrated that RNA polymerase II (Pol II)-dependent host gene transcriptions were significantly activated when RNA2.7 was removed during infection. A 145 ​nt-in-length motif within RNA2.7 was identified to inhibit the phosphorylation of Pol II Serine-2 (Pol II S2) by reducing the interaction between Pol II and phosphorylated cyclin-dependent kinase 9 (pCDK9). Due to the loss of Pol II S2 phosphorylation, cellular DNA pre-replication complex (pre-RC) factors, including Cdt1 and Cdc6, were significantly decreased, which prevented more cells from entering into S phase and facilitated viral DNA replication. Our results provide new insights of HCMV RNA2.7 functions in regulation of host cellular transcription.

摘要

人巨细胞病毒（HCMV）是一种广泛存在的病原体，属于β疱疹病毒亚科。RNA2.7 是一种高度保守的长非编码 RNA，占病毒总转录本的 20%以上。在我们的研究中，通过比较感染 HCMV 临床株和 RNA2.7 缺失突变体的细胞之间的宿主细胞转录组，研究了 HCMV RNA2.7 的功能。结果表明，当 RNA2.7 在感染过程中被去除时，RNA 聚合酶 II（Pol II）依赖性宿主基因转录明显被激活。在 RNA2.7 内鉴定出一个 145nt 长的基序，通过减少 Pol II 和磷酸化细胞周期蛋白依赖性激酶 9（pCDK9）之间的相互作用，抑制 Pol II Serine-2（Pol II S2）的磷酸化。由于 Pol II S2 磷酸化的丧失，细胞 DNA 预复制复合物（pre-RC）因子，包括 Cdt1 和 Cdc6，显著减少，这阻止了更多的细胞进入 S 期，并促进了病毒 DNA 复制。我们的研究结果为 HCMV RNA2.7 在调节宿主细胞转录中的功能提供了新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/bded62a3e18f/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/a777d1541bca/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/d8b4843ddfe6/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/03c8f5f4ad9e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/41d71fa66e93/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/bded62a3e18f/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/a777d1541bca/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/d8b4843ddfe6/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/03c8f5f4ad9e/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/41d71fa66e93/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5abb/9243627/bded62a3e18f/gr5.jpg

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