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A novel C-type lectin, perlucin, from the small abalone, Haliotis diversicolor involved in the innate immune defense against Vibrio harveyi infection. | LitMetric

A novel C-type lectin, perlucin, from the small abalone, Haliotis diversicolor involved in the innate immune defense against Vibrio harveyi infection.

Fish Shellfish Immunol

Key Laboratory of South China Sea Fishery Resources Exploitation & Utilization, Ministry of Agriculture and Rural Affairs, South China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Guangzhou, Guangdong, 510300, China. Electronic address:

Published: December 2024

C-type lectins (CTLs), a member of pattern recognition receptors, play an important role in the innate immunity by recognizing invading microorganisms. In this study, a novel perlucin gene (designated as HdPer 3), a typical CTLs was cloned and characterized from the small abalone Haliotis diversicolor. The open reading frame of HdPer 3 was 471 bp, encoding a protein of 156 amino acids that included a single carbohydrate-recognition domain. HdPer 3 was widely expressed in all tested tissues and developmental stage. HdPer 3 expression was significantly up-regulated after Vibrio harveyi infection, suggesting that HdPer 3 was activated in response to bacterial infection. The encapsulation ability of hemocytes could be significantly enhanced by the recombinant protein HdPer 3 (rHdPer 3). To understand the regulation mechanism of the HdPer 3, HdPer 3 was silenced in vivo by RNAi. Knocking down HdPer 3 decreased the hemocytes phagocytosis. Meanwhile, knocking down HdPer 3 can reduce the expression of 2 phagocytosis-related genes (Rab and Dynamin), TNF-α, and 2 MAPK pathway-related genes (MAPK-X1 and Ras) after V. harveyi infection. Moreover, HdPer 3 interference could increase the bacterial load in the hemolymph and the mortality of abalones after V. harveyi infection. All these results suggested that HdPer 3 played a crucial role in the defense against V. harveyi infection by recognizing bacterial pathogens and activating the expression of immune-related genes.

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Source
http://dx.doi.org/10.1016/j.fsi.2024.110029DOI Listing

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