Functional conservation of suppressors of cytokine signaling proteins between teleosts and mammals: Atlantic salmon SOCS1 binds to JAK/STAT family members and suppresses type I and II IFN signaling

2014 ◽  
Vol 45 (1) ◽  
pp. 177-189 ◽  
Author(s):  
Astrid Skjesol ◽  
Theresa Liebe ◽  
Dimitar B. Iliev ◽  
Ernst I.S. Thomassen ◽  
Linn Greiner Tollersrud ◽  
...  
Keyword(s):  
Atlantic Salmon ◽  
Family Members ◽  
Cytokine Signaling ◽  
Type I ◽  
Signaling Proteins ◽  
Functional Conservation ◽  
Suppressors Of Cytokine Signaling

scholarly journals Molecular Cloning and Expression Analysis of Three Suppressors of Cytokine Signaling Genes (SOCS5, SOCS6, SOCS7) in the Mealworm Beetle Tenebrio molitor

Insects ◽  
2019 ◽  
Vol 10 (3) ◽  
pp. 76 ◽  
Author(s):  
Bharat Patnaik ◽  
Bo Kim ◽  
Yong Jo ◽  
In Bang
Keyword(s):  
Functional Characterization ◽  
Tenebrio Molitor ◽  
Janus Kinase ◽  
Cloning And Expression ◽  
Cytokine Signaling ◽  
Type I ◽  
Growth Factor Signaling ◽  
Expression Levels ◽  
Mealworm Beetle ◽  
Suppressors Of Cytokine Signaling

Suppressors of cytokine signaling (SOCS) influence cytokine and growth factor signaling by negatively regulating the Janus kinase (JAK)-signal transducers and activators of transcription (STAT) pathway to maintain homeostasis during immune responses. However, functional characterization of SOCS family members in invertebrates is limited. Here, we identified and evaluated three SOCS genes (type I sub-family) in the mealworm beetle Tenebrio molitor. The full-length open reading frames (ORFs) of TmSOCS5, TmSOCS6, and TmSOCS7 comprised of 1389, 897, and 1458 nucleotides, encoding polypeptides of 462, 297, and 485 amino acids, respectively. The SH2 and SOCS box domains of the TmSOCS C-terminal region were highly conserved. Phylogenetic analysis revealed that these SOCS genes were clustered within the type I subfamily that exhibits the highest amino acid identity with Tribolium castaneum SOCS genes. Contrary to TmSOCS7 expression, the expression levels of TmSOCS5 and TmSOCS6 were lower in the larval, pupal, and adult stages. In larvae and adults, the expression levels of TmSOCS5 and TmSOCS6 were highest in the hemocytes and ovaries, respectively. SOCS transcripts were also highly upregulated in the hemocytes of T. molitor larvae within 3–6 h post-infection with the fungus Candida albicans. Collectively, these results provide valuable information regarding the involvement of TmSOCS type-I subfamily in the host immune response of insects.

scholarly journals MicroRNA gga-miR-130b Suppresses Infectious Bursal Disease Virus Replication via Targeting of the Viral Genome and Cellular Suppressors of Cytokine Signaling 5

2017 ◽  
Vol 92 (1) ◽  
Author(s):  
Mengjiao Fu ◽  
Bin Wang ◽  
Xiang Chen ◽  
Zhiyuan He ◽  
Yongqiang Wang ◽  
...  
Keyword(s):  
Disease Virus ◽  
Viral Genome ◽  
Infectious Bursal Disease Virus ◽  
Host Cells ◽  
Infectious Bursal Disease ◽  
Cytokine Signaling ◽  
Type I ◽  
Bursal Disease ◽  
Suppressors Of Cytokine Signaling

ABSTRACTMicroRNAs (miRNAs) are small noncoding RNAs that regulate gene expression posttranscriptionally through silencing or degrading their targets, thus playing important roles in the immune response. However, the role of miRNAs in the host response against infectious bursal disease virus (IBDV) infection is not clear. In this study, we show that the expression of a series of miRNAs was significantly altered in DF-1 cells after IBDV infection. We found that the miRNA gga-miR-130b inhibited IBDV replication via targeting the specific sequence of IBDV segment A and enhanced the expression of beta interferon (IFN-β) by targeting suppressors of cytokine signaling 5 (SOCS5) in host cells. These findings indicate that gga-miR-130b-3p plays a crucial role in host defense against IBDV infection.IMPORTANCEThis work shows that gga-miR-130b suppresses IBDV replication via directly targeting the viral genome and cellular SOCS5, the negative regulator for type I interferon expression, revealing the mechanism underlying gga-miR-130-induced inhibition of IBDV replication. This information will be helpful for the understanding of how host cells combat pathogenic infection by self-encoded small RNA and furthers our knowledge of the role of microRNAs in the cell response to viral infection.

scholarly journals Dietary Deoxynivalenol (DON) May Impair the Epithelial Barrier and Modulate the Cytokine Signaling in the Intestine of Atlantic Salmon (Salmo salar)

Toxins ◽  
2018 ◽  
Vol 10 (9) ◽  
pp. 376 ◽  
Author(s):  
Torfinn Moldal ◽  
Aksel Bernhoft ◽  
Grethe Rosenlund ◽  
Magne Kaldhusdal ◽  
Erling Koppang
Keyword(s):  
Atlantic Salmon ◽  
Salmo Salar ◽  
Intestinal Barrier ◽  
Production Performance ◽  
Cytokine Signaling ◽  
Control Group ◽  
Relative Expression ◽  
Distal Intestine ◽  
Atlantic Salmon Salmo Salar ◽  
Suppressors Of Cytokine Signaling

Impaired growth, immunity, and intestinal barrier in mammals, poultry, and carp have been attributed to the mycotoxin deoxynivalenol (DON). The increased use of plant ingredients in aquaculture feed implies a risk for contamination with mycotoxins. The effects of dietary DON were explored in 12-month-old Atlantic salmon (Salmo salar) (start weight of 58 g) that were offered a standard feed with non-detectable levels of mycotoxins (control group) or 5.5 mg DON/kg feed (DON group). Each group comprised two tanks with 25 fish per tank. Five fish from each tank were sampled eight weeks after the start of the feeding trial, when mean weights for the control and DON groups were 123.2 g and 80.2 g, respectively. The relative expression of markers for three tight junction proteins (claudin 25b, occludin, and tricellulin) were lower, whereas the relative expression of a marker for proliferating cell nuclear antigen was higher in both the mid-intestine and the distal intestine in fish fed DON compared with fish from the control group. The relative expression of markers for two suppressors of cytokine signaling (SOCS1 and SOCS2) were higher in the distal intestine in fish fed DON. There was no indication of inflammation attributed to the feed in any intestinal segments. Our findings suggest that dietary DON impaired the intestinal integrity, while an inflammatory response appeared to be mitigated by suppressors of cytokine signaling. A dysfunctional intestinal barrier may have contributed to the impaired production performance observed in the DON group.

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