Transcriptome-Wide Dynamics of m6A Methylation in Tumor Livers Induced by ALV-J Infection in Chickens

Transcriptome-Wide Dynamics of m6A Methylation in Tumor Livers Induced by ALV-J Infection in Chickens

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Avian Leukosis Virus Subgroup J (ALV-J) is a tumorigenic virus with high morbidity and rapid transmission.N6-methyladenosine (m6A) is a common epigenetic modification that may be closely related to the pathogenicity of ALV-J.Currently, there are no reports on whether m6A modification is related to ALV-J induced tumor formation.In this study, we used methylated RNA immunoprecipitation sequencing 2.75x100 (MeRIP-seq) and RNA sequencing (RNA-seq) to examine the differences in m6A methylation and gene expression in normal livers and ALV-J-induced tumor livers systematically, with functional enrichment and co-expression analysis.

The results identified 6,541 m6A methylated peaks, mainly enriched in CDS, and more than 83% of the transcripts contained 1-2 m6A peaks.For RNA-seq, 1,896 and 1,757 differentially expressed mRNAs and lncRNAs were identified, respectively.Gene enrichment analysis indicated that they may be involved in biological processes and pathways such as immunology-related and apoptosis.Moreover, we identified 17 lncRNAs, commonly existing in differently expressed methylome and transcriptome.

Through co-expression analysis, 126 differentially expressed lncRNAs, and 18 potentially m6A-related methyltransferases were finally identified and connected, suggesting that m6A modifications might affect gene expression of lncRNAs and play a role in ALV-J induced tumor formation.This study provides the spmx50003s50h5 first comprehensive description of the m6A expression profile in tumor livers induced by ALV-J infection in chickens, which provides a basis for studying the role of m6A modification in ALV-J induced tumorigenesis.This study provides clues for studying the epigenetic etiology and pathogenesis of ALV-J.