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Gene. 2018 Jan 10;639:27-33. doi: 10.1016/j.gene.2017.09.060. Epub 2017 Oct 2.

Toll-receptor 9 gene in the black tiger shrimp (Penaeus monodon) induced the activation of the TLR-NF-κB signaling pathway.

Author information

1
South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou 510300, China; College of Aqua-life Science and Technology, Shanghai Ocean University, Shanghai 201306, China; Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture, Guangzhou 510300, China.
2
College of Aqua-life Science and Technology, Shanghai Ocean University, Shanghai 201306, China.
3
South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou 510300, China; Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture, Guangzhou 510300, China.
4
South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou 510300, China.
5
South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou 510300, China. Electronic address: lishi_yang@yahoo.com.

Abstract

Toll receptors are important pathogen recognition receptors (PRRs) in shrimps, which play a vital role in defending against virus and bacterial challenge. In this paper, the characterization and functional analysis of a Toll9 receptor gene from Penaeus monodon was performed in HEK293T cells. Data showed that PmToll9 can activate the NF-κB promoter activities of TLR pathway, while ISRE and IFN-β promoter cannot be activated obviously in HEK293T cells using dual-luciferase reporter system. The downstream immune factors of IL-8, IκB-α, and TRAF6 were activated by PmToll9 and IL-8 showed the most significant up-regulation in expression levels, indicating the activities of NF-κB can be mediated by PmToll9. Six LRRs-deletion mutants were constructed and results showed these mutants had obvious declines in luciferase activities, among which the mutant pCMV-DeLRR4 showed the most significant decline. qPCR data indicated LRRs-deletion mutants efficiently impaired the activities of the downstream immune factors IL-8, IκB-α, and TRAF6. It demonstrates that LRRs-deletion mutants could result in the weaken abilities of PmToll9 in signaling transduction. Overexpression of PmToll9-GFP fusion protein in Hela cells revealed the primary cellular localization of PmToll9 is in the cytoplasm.

KEYWORDS:

Cell immune-model; Innate immunity; Invertebrates; LRRs-deletion mutants; Subcellular localization

PMID:
28982619
DOI:
10.1016/j.gene.2017.09.060
[Indexed for MEDLINE]

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