N6-methyladenosine RNA methylation modification regulates the transcription of viral-derived E (XSR) miRNAs to promote ALV-J replication

IF 2.4 2区 农林科学 Q3 MICROBIOLOGY
Yuqing Cao , Qingling Ren , Shuang Chang , Wenping Cui , Peng Zhao , Yixin Wang
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Abstract

The E (XSR) element located in the 3′UTR of the ALV-J genome has the capability to transcribe and generate viral-derived E (XSR) miRNA. However, the biological function and transcriptional regulation mechanism of this process remain unclear. In this study, the impact of E (XSR) miRNA on ALV-J replication and the regulatory effect of N6-methyladenosine (m6A) methylation on its transcription were investigated. The results demonstrated that E (XSR) miRNA could stimulate ALV-J replication and suppress apoptosis in DF-1 cells in vitro. E (XSR) miRNA's promotion of ALV-J replication was not associated with the type I interferon pathway, but achieved by suppressing the expression of the host GPC5 gene. The transcription of E (XSR) miRNA could be promoted by m6A methylation modification, where m6A modification was found at the A6880 and A7016 sites of ALV-J gRNA. This study provides a new perspective on the transcription of ALV-J E (XSR) miRNA and its regulatory function in ALV-J replication.

N6-甲基腺苷 RNA 甲基化修饰调控病毒源 E (XSR) miRNA 的转录,促进 ALV-J 复制
位于 ALV-J 基因组 3′UTR 的 E(XSR)元件能够转录并生成病毒衍生的 E(XSR)miRNA。然而,这一过程的生物学功能和转录调控机制仍不清楚。本研究探讨了 E (XSR) miRNA 对 ALV-J 复制的影响以及 N6-甲基腺苷(m6A)甲基化对其转录的调控作用。结果表明,E(XSR)miRNA能刺激体外DF-1细胞中ALV-J的复制并抑制其凋亡。E(XSR)miRNA对ALV-J复制的促进作用与I型干扰素途径无关,而是通过抑制宿主GPC5基因的表达实现的。E(XSR)miRNA的转录可通过m6A甲基化修饰促进,其中m6A修饰出现在ALV-J gRNA的A6880和A7016位点。这项研究为 ALV-J E (XSR) miRNA 的转录及其在 ALV-J 复制中的调控功能提供了一个新的视角。
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来源期刊
Veterinary microbiology
Veterinary microbiology 农林科学-兽医学
CiteScore
5.90
自引率
6.10%
发文量
221
审稿时长
52 days
期刊介绍: Veterinary Microbiology is concerned with microbial (bacterial, fungal, viral) diseases of domesticated vertebrate animals (livestock, companion animals, fur-bearing animals, game, poultry, fish) that supply food, other useful products or companionship. In addition, Microbial diseases of wild animals living in captivity, or as members of the feral fauna will also be considered if the infections are of interest because of their interrelation with humans (zoonoses) and/or domestic animals. Studies of antimicrobial resistance are also included, provided that the results represent a substantial advance in knowledge. Authors are strongly encouraged to read - prior to submission - the Editorials (''Scope or cope'' and ''Scope or cope II'') published previously in the journal. The Editors reserve the right to suggest submission to another journal for those papers which they feel would be more appropriate for consideration by that journal. Original research papers of high quality and novelty on aspects of control, host response, molecular biology, pathogenesis, prevention, and treatment of microbial diseases of animals are published. Papers dealing primarily with immunology, epidemiology, molecular biology and antiviral or microbial agents will only be considered if they demonstrate a clear impact on a disease. Papers focusing solely on diagnostic techniques (such as another PCR protocol or ELISA) will not be published - focus should be on a microorganism and not on a particular technique. Papers only reporting microbial sequences, transcriptomics data, or proteomics data will not be considered unless the results represent a substantial advance in knowledge. Drug trial papers will be considered if they have general application or significance. Papers on the identification of microorganisms will also be considered, but detailed taxonomic studies do not fall within the scope of the journal. Case reports will not be published, unless they have general application or contain novel aspects. Papers of geographically limited interest, which repeat what had been established elsewhere will not be considered. The readership of the journal is global.
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