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Chicken PRMT1 promotes infectious bursal disease virus replication via suppressing IFN-β production

生物 病毒复制 病毒 传染性法氏囊病 异位表达 病毒学 细胞培养 干扰素 野生型 细胞生物学 分子生物学 基因 遗传学 毒力 突变体
作者
Xifeng Hu,Xiangdong Wu,Zheng Chen,Huansheng Wu
出处
期刊:Developmental and Comparative Immunology [Elsevier]
卷期号:141: 104628-104628 被引量:6
标识
DOI:10.1016/j.dci.2022.104628
摘要

The protein arginine methyltransferase (PRMT) family, such as PRMT1, regulates the arginine methylation of various substrates. Many studies have examined the role of PRMT1 in mammals, however, it is still unknown how PRMT1 works in chickens. To investigate the effect of chicken PRMT1 (chPRMT1) on regulating IFN-β production and IBDV replication, chPRMT1 knock out DF-1 cells were constructed in this study. First, we found that chPRMT1 was widely expressed in a variety of chicken tissues and that it was distributed in the cytoplasm and nucleus of DF-1 cells. Additionally, IFN-β activation was inhibited by chPRMT1 at the step of chMAVS. In addition, chPRMT1 knock out DF-1 cells were constructed using CRISPR-Cas9 technique. The morphology and viability of chPRMT1 knock out DF-1 cells were similar with the wild-type cells. In addition, the IFN-β as well as interferon stimulate genes activation induced by chMAVS in PRMT1 knock out DF-1 cells were significantly higher than that in WT cells. Furthermore, ectopic expression of chPRMT1 significantly supports IBDV replication. We also found that the ability of IBDV replication in PRMT1 knock out DF-1 cells was remarkably lower than that of in WT cells, suggesting that PRMT1 negatively regulate IBDV replication via suppressing IFN-β production. In conclusion, the PRMT1 knock out DF-1 cells were constructed, which was further used to demonstrate an inhibitory role of chPRMT1 in IFN-β production, and a contributor of chPRMT1 in IBDV replication.
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