The regulatory mechanisms of IRF7 mediated by the type I IFN signalling pathway against Streptococcus iniae in yellowfin seabream, Acanthopagrus latus (Hottuyn, 1782)
文献类型： 外文期刊
作者： Guo, Hua-Yang 1 ; He, Hong-Xi 1 ; Liu, Bao-Suo 1 ; Zhang, Nan 1 ; Zhu, Ke-Cheng 1 ; Zhang, Dian-Chang 1 ;
作者机构： 1.Chinese Acad Fishery Sci, South China Sea Fisheries Res Inst, Key Lab South China Sea Fishery Resources Exploita, Minist Agr & Rural Affairs, Guangzhou 510300, Guangdong, Peoples R China
2.Guangdong Prov Engineer Technol Res Ctr Marine Bio, Guangzhou, Guangdong, Peoples R China
3.Sanya Trop Fisheries Res Inst, Sanya, Hainan, Peoples R China
4.231 Xingang Rd West, Guangzhou 510300, Peoples R China
关键词： Acanthopagrus latus; IRF7; IFN; Point mutation; EMSA
期刊名称：INTERNATIONAL JOURNAL OF BIOLOGICAL MACROMOLECULES （ 影响因子：8.2； 五年影响因子：7.8 ）
ISSN： 0141-8130
年卷期： 2023 年 247 卷
页码：
收录情况： SCI
摘要： Interferon regulatory factor 7 (IRF7) regulates type I interferon (IFN) genes via combining to the ISRE region in the immune response against bacteria. Streptococcus iniae is one of the dominant pathogenic bacteria of yellowfin seabream, Acanthopagrus latus. However, the regulatory mechanisms of A. latus IRF7 (AlIRF7) mediated by the type I IFN signalling pathway against S. iniae was ambiguously. In the present study, IRF7, and two IFNa3s (IFNa3 and IFNa3-like) were authenticated from A. latus. The total length of AlIRF7 cDNA is 2142 bp, containing a 1314 bp open reading frame (ORF) encoding an inferred 437 amino acids (aa). Three typical regions, a serine-rich domain (SRD), a DNA-binding domain (DBD), and an IRF association domain (IAD), are conserved in AlIRF7. Furthermore, AlIRF7 is fundamentally expressed in various kinds of organs, with high levels in the spleen and liver. Additionally, S. iniae challenge promoted AlIRF7 expression in the spleen, liver, kidney, and brain. AlIRF7 is confirmed to be located at the nucleus and cytoplasm by overexpression of AlIRF7. Moreover, truncation mu-tation analyses shows that the regions,-821 bp to +192 bp and-928 bp to +196 bp, were known as core promoters from AlIFNa3 and AlIFNa3-like, respectively. The point mutation analyses and electrophoretic mobile shift assay (EMSA) verified that AlIFNa3 and AlIFNa3-like transcriptions are depended on the M2/5 and M2/3/4 binding sites with AlIRF7 regulation, respectively. Additionally, an overexpression experiment showed that AlIRF7 can dramatically decrease the mRNA levels of two AlIFNa3s and interferon signalling molecules. These results suggest that two IFNa3s may mediate the regulation of AlIRF7 in the immune responses of A. latus against S. iniae infection.
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