Characterization and Expression Analysis of the C-Type Lectin Ladderlectin in Litopenaeus vannamei Post-WSSV Infection
文献类型： 外文期刊
作者： Xue, Qian 1 ; Yang, Bingbing 1 ; Luo, Kun 1 ; Luan, Sheng 1 ; Kong, Jie 1 ; Fu, Qiang 1 ; Cao, Jiawang 1 ; Chen, Baolong 1 ; Dai, Ping 1 ; Xing, Qun 3 ; Li, Xupeng 1 ; Meng, Xianhong 1 ;
作者机构： 1.Chinese Acad Fishery Sci, Yellow Sea Fisheries Res Inst, State Key Lab Mariculture Biobreeding & Sustainabl, Qingdao 266071, Peoples R China
2.Qingdao Marine Sci & Technol Ctr, Lab Marine Fisheries Sci & Food Prod Proc, Qingdao 266237, Peoples R China
3.BLUP Aquabreed Co Ltd, Weifang 261311, Peoples R China
关键词：
期刊名称：BIOLOGY-BASEL （ 影响因子：3.5； 五年影响因子：4.0 ）
ISSN：
年卷期： 2024 年 13 卷 10 期
页码：
收录情况： SCI
摘要： Simple Summary The outbreak of white spot syndrome poses a significant threat to the shrimp farming industry. To explore the interaction between Litopenaeus vannamei and the pathogenic white spot syndrome virus (WSSV), this study cloned and analyzed an important pattern recognition receptor, the C-type lectin ladderlectin (LvLL). The results revealed that LvLL in L. vannamei promoted WSSV replication, thereby affecting shrimp survival rates. This study demonstrated the role of LvLL in the resistance of L. vannamei to WSSV, providing theoretical insights into the mechanisms of shrimp resistance to the virus.Abstract C-type lectins are known for agglutination activity and play crucial roles in regulating the prophenoloxidase (proPO) activation system, enhancing phagocytosis and encapsulation, synthesizing antimicrobial peptides, and mediating antiviral immune responses. This work cloned a C-type lectin, ladderlectin (LvLL), from Litopenaeus vannamei. LvLL comprised a 531 bp open reading frame (ORF) that encoded 176 amino acids. The predicted LvLL protein included a signal peptide and a CLECT domain. LvLL was predicted to feature a transmembrane region, suggesting it may be a transmembrane protein. LvLL was predominantly expressed in the shrimp's hepatopancreas. After WSSV infection, LvLL expression in the hepatopancreas increased significantly by 11.35-fold after 228 h, indicating a general upregulation. Knockdown of LvLL resulted in a significant decrease in WSSV viral load and a notable increase in shrimp survival rates. Additionally, knockdown of LvLL led to a significant downregulation of apoptosis-related genes Bcl-2 and caspase 8 and a significant upregulation of p53 and proPO in WSSV-infected shrimp. This study showed that LvLL played a vital role in the interaction between L. vannamei and WSSV.
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