Nakamoto Masatoshi, Takeuchi Yusuke, Akita Kazuki, Kumagai Ryo, Suzuki Junpei, Koyama Takashi, Noda Tsutomu, Yoshida Kazunori, Ozaki Akiyuki, Araki Kazuo, Sakamoto Takashi
Department of Aquatic Marine Biosciences, Tokyo University of Marine Science and Technology, Tokyo 108-8477, Japan.
Goto Laboratory of the Seikai National Fisheries Research Institute, Japan Fisheries Research and Education Agency, Nagasaki 853-0508, Japan.
Dev Comp Immunol. 2017 Nov;76:361-369. doi: 10.1016/j.dci.2017.07.010. Epub 2017 Jul 10.
Little is known about mechanisms of resistance to parasitic diseases in marine finfish. Benedenia disease is caused by infection by the monogenean parasite Benedenia seriolae. Previous quantitative trait locus (QTL) analyses have identified a major QTL associated with resistance to Benedenia disease in linkage group Squ2 of the Japanese yellowtail/amberjack Seriola quinqueradiata. To uncover the bioregulatory mechanism of Benedenia disease resistance, complete Illumina sequencing of BAC clones carrying genomic DNA for the QTL region in linkage group Squ2 was performed to reveal a novel C-type lectin in this region. Expression of the mRNA of this C-type lectin was detected in skin tissue parasitized by B. seriolae. Scanning for single nucleotide polymorphisms (SNPs) uncovered a SNP in the C-type lectin/C-type lectin-like domain that was significantly associated with B. seriolae infection levels. These results strongly suggest that the novel C-type lectin gene controls resistance to Benedenia disease in Japanese yellowtails.
对于海洋硬骨鱼对寄生虫病的抗性机制，人们了解甚少。贝内登虫病是由单殖吸虫寄生虫贝内登虫感染引起的。先前的数量性状基因座（QTL）分析已经在日本黄尾鰤/五条鰤Seriola quinqueradiata的连锁群Squ2中确定了一个与贝内登虫病抗性相关的主要QTL。为了揭示贝内登虫病抗性的生物调节机制，对携带连锁群Squ2中QTL区域基因组DNA的BAC克隆进行了Illumina全测序，以揭示该区域中的一种新型C型凝集素。在被贝内登虫寄生的皮肤组织中检测到了这种C型凝集素mRNA的表达。对单核苷酸多态性（SNP）的扫描发现，C型凝集素/C型凝集素样结构域中的一个SNP与贝内登虫感染水平显著相关。这些结果有力地表明，这种新型C型凝集素基因控制着日本黄尾鰤对贝内登虫病的抗性。
