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G 蛋白偶联磺甲酰基神经肽受体的激活抑制埃及伊蚊的吸血行为。

Activation of the G protein-coupled sulfakinin receptor inhibits blood meal intake in the mosquito Aedes aegypti.

机构信息

Laboratory of Tropical Veterinary Medicine and Vector Biology, School of Life Sciences, Hainan University, Haikou, Hainan, China.

Hainan Province Key Laboratory of One Health, Collaborative Innovation Center of One Health, Hainan University, Haikou, Hainan, China.

出版信息

FASEB J. 2024 Aug 15;38(15):e23864. doi: 10.1096/fj.202401165R.

DOI:10.1096/fj.202401165R
PMID:39109513
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11607638/
Abstract

Little is known about the blood-feeding physiology of arbovirus vector Aedes aegypti although this type of mosquito is known to transmit infectious diseases dengue, Zika, yellow fever, and chikungunya. Blood feeding in the female A. aegypti mosquito is essential for egg maturation and for transmission of disease agents between human subjects. Here, we identify the A. aegypti sulfakinin receptor gene SKR from the A. aegypti genome and show that SKR is expressed at different developmental stages and in varied anatomical localizations in the adult mosquito (at three days after eclosion), with particularly high expression in the CNS. Knockingdown sulfakinin and sulfakinin receptor gene expression in the female A. aegypti results in increased blood meal intake, but microinjection in the thorax of the sulfakinin peptide 1 and 2 both inhibits dose dependently blood meal intake (and delays the time course of blood intake), which is reversible with receptor antagonist. Sulfakinin receptor expressed ectopically in mammalian cells CHO-K1 responds to sulfakinin stimulation with persistent calcium spikes, blockable with receptor antagonist. These data together suggest that activation of the Gq protein-coupled (i.e., calcium-mobilizing) sulfakinin receptor inhibits blood meal intake in female A. aegypti mosquitoes and could serve as a strategic node for the future control of A. aegypti mosquito reproduction/population and disease transmission.

摘要

关于黄病毒媒介埃及伊蚊的吸血生理学知之甚少，尽管这种蚊子已知会传播登革热、寨卡、黄热病和基孔肯雅热等传染病。雌性埃及伊蚊的吸血对于卵成熟和在人类宿主之间传播疾病病原体是必不可少的。在这里，我们从埃及伊蚊基因组中鉴定出埃及伊蚊磺肽受体基因 SKR，并表明 SKR 在成年蚊子（出茧后三天）的不同发育阶段和不同解剖部位表达，在中枢神经系统中表达特别高。在雌性埃及伊蚊中敲低磺肽和磺肽受体基因表达会导致血液摄入量增加，但胸腔内注射磺肽 1 和 2 均可剂量依赖性地抑制血液摄入量（并延迟血液摄入的时间过程），受体拮抗剂可使其逆转。在哺乳动物细胞 CHO-K1 中异位表达的磺肽受体对磺肽刺激产生持续的钙峰反应，可用受体拮抗剂阻断。这些数据共同表明，激活 Gq 蛋白偶联（即钙动员）的磺肽受体可抑制雌性埃及伊蚊的血液摄入量，并可作为未来控制埃及伊蚊繁殖/种群和疾病传播的战略节点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/d3319461a10a/FSB2-38-e23864-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/54549ca8ff01/FSB2-38-e23864-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/89ea8d50c80d/FSB2-38-e23864-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/c4b58d6f9032/FSB2-38-e23864-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/9ea8e4a442d1/FSB2-38-e23864-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/da20026b9ed9/FSB2-38-e23864-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/d3319461a10a/FSB2-38-e23864-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/54549ca8ff01/FSB2-38-e23864-g007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/89ea8d50c80d/FSB2-38-e23864-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/c4b58d6f9032/FSB2-38-e23864-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/9ea8e4a442d1/FSB2-38-e23864-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/da20026b9ed9/FSB2-38-e23864-g008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e686/11607638/d3319461a10a/FSB2-38-e23864-g004.jpg

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