Abstract

The suppressors of cytokine signaling (SOCS) family are important soluble mediators to inhibit signal transduction via the Janus kinase/signal transducer and activator of transcription (JAK-STAT) pathway in the innate and adaptive immune responses. SOCS1 is the primary regulator of a number of cytokines. In this study, two spliced transcripts of SOCS1 were identified and characterized from black rockfish (Sebastes schlegeli), named SsSOCS1a and SsSOCS1b. SsSOCS1a and SsSOCS1b contained conserved structural and functional domains including KIR region, ESS region, SH2 domain and SOCS box. SsSOCS1a and SsSOCS1b were distributed ubiquitously in all the detected tissues with the higher expression level in liver and spleen. After stimulation in vivo with Vibrio anguillarum and Edwardsiella tarda, the mRNA expression of SsSOCS1a and SsSOCS1b were induced in most of the immune-related tissues, including head kidney, spleen and liver. Meanwhile, poly I:C and IFNγ up-regulated the expression of SsSOCS1a and SsSOCS1b that reached the highest level at 24 h in macrophages in vitro. Luciferase assays in HEK293 cells showed SsSOCS1a and SsSOCS1b had the similar function in inhibiting ISRE activity after poly I:C and IFNγ treatment. Furthermore, KIR domain in black rockfish was determined to have a negative regulatory role in IFN signaling. SsSOCS1a and SsSOCS1b were found to interact strongly with each other by Co-immunoprecipitation analyses. These results indicated that the function of SOCS1 in the negative regulation of IFN signaling is conserved from teleost to mammals which will be helpful to further understanding of the biological functions of teleosts SOCS1 in innate immunity.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.