4.4 Article

Molecular analysis of chicken interferon-alpha inducible protein 6 gene and transcriptional regulation

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JOURNAL OF ANIMAL SCIENCE AND TECHNOLOGY
卷 65, 期 1, 页码 183-196

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KOREAN SOCIETY ANIMAL SCIENCE & TECHNOLOGY
DOI: 10.5187/jast.2022.e101

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Interferon-alpha inducible protein 6 gene; Avian influenza virus; Toll-like receptor 3 signaling pathway; NF-kappa B pathway; MAPKs pathway; DF-1 cells

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In this study, the chicken IFI6 gene (chIFI6) was identified and its transcriptional regulation in HPAIV-infected chickens was studied. It was found that the expression of chIFI6 was significantly increased in the lungs, spleens, and tracheas of HPAIV-infected chickens compared to the control group. TLR3 signals were found to regulate the transcription of chIFI6 in chicken cells.
Interferon-alpha inducible protein 6 (IFI6) is an interferon-stimulated gene (ISG), belonging to the FAM14 family of proteins and is localized in the mitochondrial membrane, where it plays a role in apoptosis. Transcriptional regulation of this gene is poorly understood in the context of inflammation by intracellular nucleic acid-sensing receptors and pathological conditions caused by viral infection. In this study, chicken IFI6 (chIFI6) was identified and studied for its molecular features and transcriptional regulation in chicken cells and tissues, i.e., lungs, spleens, and tracheas from highly pathogenic avian influenza virus (HPAIV)-infected chickens. The chIFI6-coding sequences contained 1638 nucleotides encoding 107 amino acids in three exons, whereas the duck IFI6-coding sequences contained 495 nucleotides encoding 107 amino acids. IFI6 proteins from chickens, ducks, and quail contain an IF6/IF27-like superfamily domain. Expression of chIFI6 was higher in HPAIV-infected White Leghorn chicken lungs, spleens, and tracheas than in mock-infected controls. TLR3 signals regulate the transcription of chIFI6 in chicken DF-1 cells via the NF-.B and JNK signaling pathways, indicating that multiple signaling pathways differentially contribute to the transcription of chIFI6. Further research is needed to unravel the molecular mechanisms underlying IFI6 transcription, as well as the involvement of chIFI6 in the pathogenesis of HPAIV in chickens.

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