Yuan Kai, Yuan Feng-Hua, Weng Shao-Ping, He Jian-Guo, Chen Yi-Hong
School of Life Sciences, Sun Yat-sen University, 135 Xingang Road West, Guangzhou 510275, PR China; State Key Laboratory for Biocontrol, MOE Key Laboratory of Aquatic Product Safety, Institute of Aquatic Economic Animals and Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-sen University, 135 Xingang Road West, Guangzhou 510275, PR China.
Key Laboratory of Marine Resources and Coastal Engineering in Guangdong Province, South China Sea Bio-Resource Exploitation and Protection Collaborative Innovation Center (SCS-REPIC), School of Marine Sciences, Sun Yat-sen University, 135 Xingang Road West, Guangzhou 510275, PR China; School of Life Sciences, Sun Yat-sen University, 135 Xingang Road West, Guangzhou 510275, PR China; State Key Laboratory for Biocontrol, MOE Key Laboratory of Aquatic Product Safety, Institute of Aquatic Economic Animals and Guangdong Province Key Laboratory for Aquatic Economic Animals, Sun Yat-sen University, 135 Xingang Road West, Guangzhou 510275, PR China.
Dev Comp Immunol. 2017 Mar;68:46-57. doi: 10.1016/j.dci.2016.11.016. Epub 2016 Nov 21.
Shrimp innate immunity is the first line of resistance against pathogenic bacteria. The Toll-like receptor (TLR)-NF-κB pathway is vital in this immunity process. In this study, a novel Spätzle gene (LvSpz4) of Litopenaeus vannamei was cloned and functionally characterized. The open reading frame of LvSpz4 was 918 bp, which encoded a putative protein with 305 amino acids. LvSpz4 was most expressed in the gills of L. vannamei. This expression was induced by Vibrio alginolyticus or Staphylococcus aureus infection or lipopolysaccharide stimulation. The reporter gene assay showed that LvSpz4 could activate the promoters of Pen4, Drs, AttA, Mtk, and white spot syndrome virus immediate early gene1 in Drosophila Schneider 2 (S2) cells. Knockdown LvSpz4 increased the cumulative mortality of L. vannamei upon V. alginolyticus infection. The unfolded protein response (UPR) induced the expression of LvSpz4 in L. vannamei. Moreover, the promoter of LvSpz4 was activated by L. vannamei X-Box binding protein 1 and activating transcription factor 4 in S2 cells. These results suggested that LvSpz4 was involved in L. vannamei innate immunity and caused the crosstalk between the TLR-NF-κB pathway and UPR.
对虾的先天免疫是抵御病原菌的第一道防线。Toll样受体(TLR)-NF-κB信号通路在这一免疫过程中至关重要。在本研究中,克隆了凡纳滨对虾一个新的斯帕茨勒基因(LvSpz4)并对其进行了功能鉴定。LvSpz4的开放阅读框为918 bp,编码一个含有305个氨基酸的推定蛋白。LvSpz4在凡纳滨对虾的鳃中表达量最高。这种表达可由溶藻弧菌或金黄色葡萄球菌感染或脂多糖刺激诱导。报告基因检测表明,LvSpz4可在果蝇Schneider 2(S2)细胞中激活Pen4、Drs、AttA、Mtk和白斑综合征病毒立即早期基因1的启动子。敲低LvSpz4会增加凡纳滨对虾在溶藻弧菌感染后的累计死亡率。未折叠蛋白反应(UPR)诱导凡纳滨对虾中LvSpz4的表达。此外,LvSpz4的启动子在S2细胞中被凡纳滨对虾X盒结合蛋白1和激活转录因子4激活。这些结果表明,LvSpz4参与了凡纳滨对虾的先天免疫,并导致了TLR-NF-κB信号通路与UPR之间的相互作用。