Janus激酶(JAK)信号转导和转录激活因子(STAT)途径已被证明可以控制各种生理过程,包括免疫反应,造血,细胞生长,和差异化。最近的研究表明,细胞因子信号抑制蛋白(SOCS)减弱哺乳动物的JAK-STAT信号;然而,它们在鳞翅目昆虫中的功能不太清楚。这里,我们报告了来自中国橡树蚕的SOCS-2的全长序列(称为ApSOCS-2),并研究了其通过JAK-STAT途径在免疫应答中的生物学作用。ApSOCS-2在Pernyi五龄幼虫的脂肪体和血细胞中表达较高。病原体感染核型多角体病毒后,白僵菌,大肠杆菌,和黄体Microcus,与对照组相比,ApSOCS-2mRNA显著增加。为了阐明先天免疫的可能参与,我们测量了pernyi脂肪体中抗菌肽基因的表达谱。相比之下,重组ApSOCS-2蛋白给药显着降低了AMPs的转录,而RNAi对ApSOCS-2的消耗增加了它们的表达。此外,我们在dsApSOCS-2处理的幼虫中观察到更高的抗菌活性和更低的细菌复制。在被黄体分枝杆菌攻击的STAT耗尽的a虫幼虫中,ApSOCS-2转录水平降低。ApSOCS-2RNAi数据集也进行了转录组学分析,这表明ApSOCS-2是免疫功能的关键调节因子。一起来看,我们的数据表明,ApSOCS-2是昆虫中通过JAK-STAT途径负调节AMPs转录本所必需的。
The Janus kinase (JAK) signal transducer and activator of transcription (STAT) pathway has been shown to govern various physiological processes, including immune responses, hematopoiesis, cell growth, and differentiation. Recent studies show that suppressors of cytokine signaling (SOCS) proteins attenuate JAK-STAT signaling in mammals; however, their functions are less clear in lepidopteran insects. Here, we report a full-length sequence of SOCS-2 from the Chinese oak silkworm Antheraea pernyi (designated as ApSOCS-2) and study its biological role in immune responses via the JAK-STAT pathway. ApSOCS-2 expression was high in the fat bodies and hemocytes of A. pernyi fifth instar larvae. After pathogen infection with nucleopolyhedrovirus, Beauveria bassiana, Escherichia coli, and Microccus luteus, ApSOCS-2 mRNA was strongly increased compared to the control group. To elucidate the possible involvement in innate immunity, we measured antimicrobial peptide genes expression profiles in the fat body of A. pernyi. In contrast, recombinant ApSOCS-2 protein administration significantly reduced the AMPs transcription, while the depletion of ApSOCS-2 by RNAi increased their expression. Furthermore, we observed higher antibacterial activity and lower bacterial replication in dsApSOCS-2-treated larvae. The ApSOCS-2 transcription level was reduced in STAT depleted A. pernyi larvae challenged by M. luteus. The ApSOCS-2 RNAi data sets were also subjected to transcriptomic analysis, which suggests that ApSOCS-2 is a key regulator of immune function. Taken together, our data suggest that ApSOCS-2 is required for the negative regulation of AMPs transcripts via the JAK-STAT pathway in the insect.