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C型凝集素连接埃及伊蚊的免疫和生殖过程。

C-Type Lectins Link Immunological and Reproductive Processes in Aedes aegypti.

作者信息

Li Hsing-Han, Cai Yu, Li Jian-Chiuan, Su Matthew P, Liu Wei-Liang, Cheng Lie, Chou Shu-Jen, Yu Guann-Yi, Wang Horng-Dar, Chen Chun-Hong

机构信息

Institution of Biotechnology, National Tsing Hua University, Hsinchu, 300044, Taiwan; National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, Miaoli 350401, Taiwan.

Temasek Life Sciences Laboratory, National University of Singapore, 117604, Singapore; Department of Biological Sciences, National University of Singapore, 117558, Singapore.

出版信息

iScience. 2020 Aug 21;23(9):101486. doi: 10.1016/j.isci.2020.101486.

DOI:10.1016/j.isci.2020.101486
PMID:32891883
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7481239/
Abstract

Physiological trade-offs between mosquito immune response and reproductive capability can arise due to insufficient resource availability. C-type lectin family members may be involved in these processes. We established a GCTL-3 mutant Aedes aegypti using CRISPR/Cas9 to investigate the role of GCTL-3 in balancing the costs associated with immune responses to arboviral infection and reproduction. GCTL-3 mutants showed significantly reduced DENV-2 infection rate and gut commensal microbiota populations, as well as upregulated JAK/STAT, IMD, Toll, and AMPs immunological pathways. Mutants also had significantly shorter lifespans than controls and laid fewer eggs due to defective germ line development. dsRNA knock-down of Attacin and Gambicin, two targets of the AMPs pathway, partially rescued this reduction in reproductive capabilities. Upregulation of immune response following GCTL-3 knock-out therefore comes at a cost to reproductive fitness. Knock-out of other lectins may further improve our knowledge of the molecular and genetic mechanisms underlying reproduction-immunity trade-offs in mosquitoes.

摘要

由于资源可用性不足,蚊子的免疫反应和生殖能力之间可能会出现生理权衡。C型凝集素家族成员可能参与这些过程。我们使用CRISPR/Cas9技术建立了GCTL-3突变型埃及伊蚊,以研究GCTL-3在平衡与虫媒病毒感染免疫反应和生殖相关成本中的作用。GCTL-3突变体的登革热病毒2型感染率和肠道共生微生物群数量显著降低,同时JAK/STAT、IMD、Toll和抗菌肽免疫途径上调。由于生殖系发育缺陷,突变体的寿命也明显短于对照组,产卵数量也更少。抗菌肽途径的两个靶点Attacin和Gambicin的dsRNA敲低部分挽救了这种生殖能力的下降。因此,GCTL-3敲除后免疫反应的上调是以生殖适应性为代价的。敲除其他凝集素可能会进一步增进我们对蚊子生殖-免疫权衡背后分子和遗传机制的了解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/5fe47080f71e/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/b861e708e4d2/fx1.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/be4f914cb10b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/17a7a524c861/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/56d96d535002/gr4.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/f77261b7a38a/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/8e60e9e0cd94/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/5fe47080f71e/gr8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/b861e708e4d2/fx1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/e23d0b1f12ef/gr1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/be4f914cb10b/gr2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/17a7a524c861/gr3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/56d96d535002/gr4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/256fdc3991de/gr5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/f77261b7a38a/gr6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/8e60e9e0cd94/gr7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0b25/7481239/5fe47080f71e/gr8.jpg

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