Abstract
Transmissible gastroenteritis virus (TGEV) is a porcine pathogen causing highly communicable gastrointestinal infection that are lethal for suckling piglets. In an attempt to delineate the pathogenic mechanism of TGEV-infected porcine testicular cells (ST cells), we conducted a whole genome analysis of DNA methylation and expression in ST cells through reduced bisulfate-seq and RNA-seq. We examined alterations in the methylation patterns and recognized 1764 distinct methylation sites. 385 differentially expressed genes (DEGs) were enriched in the viral defense and ribosome biogenesis pathways. Integrative analysis identified two crucial genes (EMILIN2, RIPOR3), these two genes expression were negatively correlated to promoter methylation. In conclusion, alterations in DNA methylation and differential expression of genes reveal that their potential functional interactions in TGEV infection. Our data highlights the epigenetic and transcriptomic landscapes in TGEV-infected ST cells and provides a reliable dataset for screening TGEV resistance genes and genetic markers.
Highlights
DNA methylation is a widely studied mode of epigenetic modification, play a crucial role in modulating gene expression and chromatin conformation
Transmissible gastroenteritis virus (TGEV) was introduced to cells for 0, 12, 24, 48, and 72 h and cytopathic effects (CPE) was assessed
In addition to the in vivo assays and intestinal organoid culture systems [43], most of the studies against TGEV were performed via TGEV infection of cell lines in vitro
Summary
DNA methylation is a widely studied mode of epigenetic modification, play a crucial role in modulating gene expression and chromatin conformation. DNA is methylated when methyl groups are added to the 5 ’C cytosine position, in response to DNA methyltransferases [1]. DNA methylation is regarded as a reliable and accessible epigenetic marker [2]. Methylated DNA can induce diseases like dysplasia and tumors. Pathogenic bacteria, drug therapy, and food supply can alter genomic methylation status, thereby manipulating the expression of responsive genes and facilitating phenotypic consequences [3,4,5]. The study of DNA methylation is crucial for the in-depth comprehension of gene expression, ontogeny, and disease development
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