![]() Deficiency in IRF7 attenuated the elevated expression of IFNs and ISGs and restored susceptibility to RV infection in Mettl3ΔIEC mice. In the absence of METT元, IECs showed increased Irf7 mRNA stability and enhanced type I and III IFN expression. Using RNA-sequencing and m6A RNA immuno-precipitation (RIP)-sequencing, we identified IRF7, a master regulator of IFN responses, as one of the primary m6A targets during virus infection. Mice lacking the m6A writer enzymes METT元 in IECs ( Mettl3ΔIEC) were resistant to RV infection and showed increased expression of interferons (IFNs) and IFN-stimulated genes (ISGs). We found that rotavirus infection induced global m6A modifications on mRNA transcripts by down-regulating the m6a eraser ALKBH5. Here, we uncover a novel antiviral function of m6A modification during rotavirus (RV) infection in small bowel intestinal epithelial cells (IECs). However, how m6A levels are regulated during physiological or pathological processes such as virus infections, and the in vivo function of m6A in the intestinal immune defense against virus infections are largely unknown. N6-methyladenosine (m6A) is an abundant mRNA modification and affects many biological processes. Institute of Health and Medicine, Hefei Comprehensive National Science Center, Hefei, China, China.School of Data Science, University of Science and Technology of China, China.Howard Hughes Medical Institute, Yale University School of Medicine, United States.Department of Immunobiology, Yale University School of Medicine, United States.Department of Molecular Microbiology, Washington University School of Medicine in St.Shanghai Institute of Immunology, Department of Microbiology and Immunology, Shanghai Jiao Tong University School of Medicine (SJTU-SM), China.Institute of Immunology, the Chinese Academy of Sciences Key Laboratory of Innate Immunity and Chronic Disease, Division of Life Sciences and Medicine, University of Science and Technology of China, China.Department of Digestive Disease, The First Affiliated Hospital of University of Science and Technology of China, Division of Life Sciences and Medicine, University of Science and Technology of China, China. ![]()
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