Complement-like protein TEP1 is a determinant of vectorial capacity in the malaria vector Anopheles gambiae
Complement-like protein TEP1 is a determinant of vectorial capacity in the malaria vector Anopheles gambiae
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DOI：
10.1016/s0092-8674(04)00173-4
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发表时间：
2004-03-05
期刊：
影响因子：
64.5
通讯作者：
Levashina, EA
中科院分区：
文献类型：
--
作者：
Blandin, S;Shiao, SH;Levashina, EA
按蚊是非洲人类疟疾的主要传播媒介。蚊子作为媒介和传播疟疾寄生虫的能力存在很大差异，但决定媒介能力的分子机制仍然知之甚少。我们报道了冈比亚按蚊的血细胞特异性补体样蛋白 TEP1 与啮齿类疟疾寄生虫伯氏疟原虫的中肠阶段结合并介导杀灭。成人中 TEP1 的 dsRNA 敲低完全消除了基因选择的难治性菌株中的黑色素难治性。此外，在易感蚊子中，这种敲低增加了正在发育的寄生虫的数量。我们的结果表明，TEP1 依赖性寄生虫杀死之后，通过裂解和/或黑化作用，TEP1 独立地清除死亡寄生虫。进一步阐明TEP1介导的杀灭寄生虫的分子机制对于我们理解昆虫媒介能力的原理具有重要意义。
Anopheles mosquitoes are major vectors of human malaria in Africa. Large variation exists in the ability of mosquitoes to serve as vectors and to transmit malaria parasites, but the molecular mechanisms that determine vectorial capacity remain poorly understood. We report that the hemocyte-specific complement-like protein TEP1 from the mosquito Anopheles gambiae binds to and mediates killing of midgut stages of the rodent malaria parasite Plasmodium, berghei. The dsRNA knockdown of TEP1 in adults completely abolishes melanotic refractoriness in a genetically selected refractory strain, Moreover, in susceptible mosquitoes this knockdown increases the number of developing parasites. Our results suggest that the TEP1-dependent parasite killing is followed by a TEP1-independent clearance of dead parasites by lysis and/or melanization. Further elucidation of the molecular mechanisms of TEP1-mediated parasite killing will be of great importance for our understanding of the principles of vectorial capacity in insects.