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| 海洋贝类Toll样受体及其接头蛋白MyD88的分子进化研究 |
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王璐1,2,3,4, 产久林1,2,3, 李倩1,2,3,4, 张琳琳1,2,3
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1.中国科学院海洋研究所 实验海洋生物学重点实验室 青岛 266071;2.中国科学院海洋大科学研究中心 青岛 266071;3.青岛海洋科学与技术试点国家实验室 海洋生物学与生物技术功能实验室 青岛 266237;4.中国科学院大学 北京 100049
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| 摘要: |
| 海洋贝类在长期的进化过程中具备了复杂和独特的免疫体系，为免疫防御系统的适应性进化研究提供了典型实例。目前海洋贝类天然免疫系统经典分子在后生动物演化历程中的特点尚不明确。为探究模式识别受体Toll样受体（TLR）及其接头分子髓样分化因子（MyD88）基因家族在后生动物中的进化历程，研究了32个后生动物演化代表性物种中TLR及MyD88基因家族的系统发育关系，以长牡蛎为代表物种探讨了长牡蛎TLRs和MyD88s在病原感染、环境胁迫、早期发育和组织分化条件下的基因表达模式。结果表明，海洋贝类中普遍存在TLR和MyD88基因家族的扩张，在腹足类和双壳类中检测到两个基因家族谱系特异性的基因扩张，46个长牡蛎特异性扩张的TLR基因能够被病原诱导表达，且在不同类型的病原感染下，其表达模式具有特异性。和病原诱导表达的TLRs相比，参与牡蛎早期发育的TLRs起源相对古老。研究结果表明，海洋贝类天然免疫模式识别受体TLR及其接头分子MyD88通过基因复制和表达分化形成了复杂特异的信号传导通路，这有助于深入了解海洋贝类的天然免疫防御系统的特点，丰富后生动物天然免疫进化的脉络。 |
| 关键词: 分子进化 TLR信号通路 天然免疫 功能分化 软体动物 长牡蛎 |
| DOI：10.11693/hyhz20210200041 |
| 分类号:S917.4 |
| 基金项目:中国科学院B类战略先导科技专项，XDB42000000号；国家自然科学基金面上项目，41976088号；中国科学院海洋大科学研究中心重点部署项目，COMS2019R01号；青岛海洋科学与技术试点国家实验室海洋生物学与生物技术功能实验室引进人才支持计划项目，YJ2019NO01号。 |
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| EVOLUTIONARY HISTORY OF THE TOLL-LIKE RECEPTOR AND MYD88 IN MOLLUSCS |
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WANG Lu1,2,3,4, CHAN Jiu-Lin1,2,3, LI Qian1,2,3,4, ZHANG Lin-Lin1,2,3
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1.Key Laboratory of Experimental Marine Biology, Institute of Oceanology, Chinese Academy of Sciences, Qingdao 266071, China;2.Center for Ocean Mega-Science, Chinese Academy of Sciences, Qingdao 266071, China;3.Laboratory for Marine Biology and Biotechnology, Pilot National Laboratory for Marine Science and Technology(Qingdao), Qingdao 266237, China;4.University of Chinese Academy of Sciences, Beijing 100049, China
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| Abstract: |
| To adapt to a wide range of pathogenic environment, marine molluscs have developed a unique innate immune system in evolution. The toll-like receptors (TLR) and their adaptor MyD88 are ancient molecular components in animals and are best known for their roles in defense against pathogenic microorganisms. To deepen understanding of mollusk TLR signaling pathway, the evolutionary history of molluscan TLR and its adaptor MyD88 in 32 species was studied, and the gene expression patterns of TLRs and MyD88s in Crassostrea gigas under different conditions were explored. Molluscs expanded genes coding for TLR and MyD88 extensively as shown in phylogeny analysis. In C. gigas, 46 specifically expanded TLRs could be activated by pathogens, and their expression patterns were specific to the types of pathogen infection. Compared with pathogen-induced TLRs, the origin of TLRs involved in early development of oyster is relatively ancient in evolution. This study provided a basis for deep understanding of innate immunity of molluscs and the evolution of invertebrate innate immunity. |
| Key words: molecular evolution TLR signaling pathway innate immunity functional divergence molluscs Crassostrea gigas |