Two IFNa3s mediate the regulation of IRF9 in the process of infection with Streptococcus iniae in yellowfin seabream, Acanthopagrus latus (Hottuyn, 1782)
文献类型： 外文期刊
作者： He, Hong-Xi 1 ; Guo, Hua-Yang 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, Peoples R China
2.Guangdong Prov Engineer Technol Res Ctr Marine Bio, Guangzhou 510300, Peoples R China
3.Sanya Trop Fisheries Res Inst, Sanya 510300, Peoples R China
关键词： Acanthopagrus latus; IRF9; IFN; Subcellular localization
期刊名称：DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY （ 影响因子：2.9； 五年影响因子：3.1 ）
ISSN： 0145-305X
年卷期： 2024 年 156 卷
页码：
收录情况： SCI
摘要： IRF9 can play an antibacterial role by regulating the type I interferon (IFN) pathway. Streptococcus iniae can cause many deaths of yellowfin seabream, Acanthopagrus latus in pond farming. Nevertheless, the regulatory mechanism of type I IFN signalling by A. latus IRF9 ( AlIRF9 ) against S. iniae remains elucidated. In our study, AlIRF9 has a total cDNA length of 3200 bp and contains a 1311 bp ORF encoding a presumed 436 amino acids (aa). The genomic DNA sequence of AlIRF9 has nine exons and eight introns, and AlIRF9 was expressed in various tissues, containing the stomach, spleen, brain, skin, and liver, among which the highest expression was in the spleen. Moreover, AlIRF9 transcriptions in the spleen, liver, kidney, and brain were increased by S. iniae infection. By overexpression of AlIRF9 , AlIRF9 is shown as a whole-cell distribution, mainly concentrated in the nucleus. Moreover, the promoter fragments of -415 to +192 bp and -311 to +196 bp were regarded as core sequences from two AlIFNa3s . The point mutation analyses verified that AlIFNa3 and AlIFNa3-like transcriptions are dependent on both M3 sites with AlIRF9 . In addition, AlIRF9 could greatly reduce two AlIFNa3s and interferon signalling factors expressions. These results showed that in A. latus , both AlIFNa3 and AlIFNa3-like can mediate the regulation of AlIRF9 in the process of infection with S. iniae .
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