# Transcriptome-Wide Identification and Analysis Reveals m6A Regulation of Porcine Intestinal Epithelial Cells Under TGEV Infection

## TL;DR

This study explores how m6A RNA modifications change in pig intestinal cells infected with TGEV, identifying key genes and pathways involved in the infection process.

## Contribution

The first systematic characterization of m6A modifications in TGEV-infected porcine intestinal cells, revealing potential antiviral targets.

## Key findings

- 14,813 m6A peaks were identified in IPEC-J2 cells, with 832 peaks and 1660 genes showing significant changes after TGEV infection.
- m6A modification levels were positively correlated with transcript expression, particularly in the mTOR signaling pathway.
- SOS2 was identified as a potential moderator in TGEV infection through PPI network and RT-qPCR analysis.

## Abstract

Transmissible gastroenteritis virus (TGEV) represents a widespread and critically pathogenic enteric pathogen that poses significant economic threats to pig production worldwide. However, the role of m6A modification in TGEV-infected host cells remains largely unexplored. In this study, we conducted a comprehensive analysis of m6A epitranscriptomic modifications in TGEV-challenged IPEC-J2 cell lines. The resulting data constitute the first systematic characterization of N6-methyladenosine landscapes in porcine intestinal cells experiencing pathogen-driven metabolic shifts, with implications for targeted therapeutic interventions against this economically significant virus.

Transmissible gastroenteritis virus (TGEV) represents a critical intestinal pathogen responsible for acute enteritis in pigs, posing significant challenges to global swine production biosecurity. N6-methyladenosine (m6A), the most abundant epitranscriptomic mark in eukaryotic messenger RNA, has emerged as a regulatory factor in host–virus interactions. Despite its recognized importance, the functional significance of m6A modifications during TGEV infection of porcine jejunal epithelial (IPEC-J2) cells remains unexplored. Here, we established a TGEV-infected IPEC-J2 cell model and we employed methylated RNA immunoprecipitation sequencing (MeRIP-seq) to comprehensively profile the m6A epitranscriptomic landscape and identify N6-methyladenosine-bearing transcripts in IPEC-J2 cells following TGEV challenge. A total of 14,813 m6A peaks were identified in the IPEC-J2, distributed in 7728 genes, mainly enriched in the CDS and 3′-UTRs. After TGEV infection, we identified 832 m6A peaks and 1660 genes with significant changes. Integrative analysis revealed a direct positive relationship between N6-methyladenosine modification abundance and transcript expression levels. Through integrated examination of MeRIP-Seq and RNA-Seq datasets, we identified 105 transcripts bearing m6A modifications, which were mainly enriched in the mTOR signaling pathway. Protein–protein interaction (PPI) network and RT-qPCR analysis demonstrated that SOS2 probably acts an important moderator in TGEV infection. This work contributes to understanding the m6A modification landscape in the TGEV-swine model and suggests SOS2 as potential target for future antiviral strategies.