期刊
RNA
卷 16, 期 2, 页码 307-315出版社
COLD SPRING HARBOR LAB PRESS, PUBLICATIONS DEPT
DOI: 10.1261/rna.1819210
关键词
microRNA; RNA silencing; small RNA profiling; herpesvirus; mouse cytomegalovirus; regulation; RNA processing
资金
- Agence Nationale pour la Recherche [ANR-07-MIME-012-01]
- CNRS
- Wellcome Trust [082611/Z/07/Z]
- Biotechnology and Biological Science Research Council [BB/G01552X/1]
- German Federal Ministry of Education and Research [01GS0801]
- Wellcome Trust [082611/Z/07/Z] Funding Source: Wellcome Trust
- Biotechnology and Biological Sciences Research Council [BB/G01552X/1] Funding Source: researchfish
- BBSRC [BB/G01552X/1] Funding Source: UKRI
In mammals, microRNAs (miRNAs) can play diverse roles in viral infection through their capacity to regulate both host and viral genes. Recent reports have demonstrated that specific miRNAs change in expression level upon infection and can impact viral production and infectivity. It is clear that miRNAs are an integral component of viral-host interactions, and it is likely that both host and virus contain mechanisms to regulate miRNA expression and/or activity. To date, little is known about the mechanisms by which miRNAs are regulated in viral infection. Here we report the rapid down-regulation of miR-27a in multiple mouse cell lines as well as primary macrophages upon infection with the murine cytomegalovirus. Down-regulation of miR-27a occurs independently from two other miRNAs, miR-23a and miR-24, located within the same genomic cluster, and analysis of pri-miRNA levels suggest that regulation occurs post-transcriptionally. miR-27b, a close homolog of miR-27a (20/21 nucleotide identity), also decreases upon infection, and we demonstrate that both miR-27a and miR-27b exert an antiviral function upon over-expression. Drug sensitivity experiments suggest that virus entry is not sufficient to induce the down-regulation of miR-27 and that the mechanism requires synthesis of RNA. Altogether, our findings indicate that miR-27a and miR-27b have antiviral activity against MCMV, and that either the virus or the host encodes molecule(s) for regulating miR-27 accumulation, most likely by inducing the rapid decay of the mature species.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据