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氨基酸依赖的胰岛素样肽信号转导调控是由疾病传播媒介蚊子中的 TOR 和 GATA 因子介导的。

Amino acid-dependent regulation of insulin-like peptide signaling is mediated by TOR and GATA factors in the disease vector mosquito .

机构信息

School of Life Science and Technology, Key Laboratory of Developmental Genes and Human Disease, Southeast University, Nanjing 210096, China.

Department of Entomology, University of California, Riverside, CA 92521.

出版信息

Proc Natl Acad Sci U S A. 2023 Aug 22;120(34):e2303234120. doi: 10.1073/pnas.2303234120. Epub 2023 Aug 14.

DOI:10.1073/pnas.2303234120
PMID:37579141
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10450652/
Abstract

female mosquitoes require vertebrate blood for their egg production and consequently they become vectors of devastating human diseases. Amino acids (AAs) and nutrients originating from a blood meal activate vitellogenesis and fuel embryo development of anautogenous mosquitoes. Insulin-like peptides (ILPs) are indispensable in reproducing female mosquitoes, regulating glycogen and lipid metabolism, and other essential functions. However, how ILPs coordinate their action in response to the AA influx in mosquito reproduction was unknown. We report here that the AA/Target of Rapamycin (TOR) signaling pathway regulates ILPs through GATA transcription factors (TFs). AA infusion combined with RNA-interference TOR silencing of revealed their differential action on ILPs, elevating circulating levels of several ILPs but inhibiting others, in the female mosquito. Experiments involving isoform-specific CRISPR-Cas9 genomic editing and chromatin immunoprecipitation assays showed that the expression of , , and genes was inhibited by the GATA repressor (GATAr) isoform in response to low AA-TOR signaling, while the expression of , , , , and genes was activated by the GATA activator isoform after a blood meal in response to the increased AA-TOR signaling. FoxO, a downstream TF in the insulin pathway, was involved in the TOR-GATAr-mediated repression of , , and genes. This work uncovered how AA/TOR signaling controls the ILP pathway in modulation of metabolic requirements of reproducing female mosquitoes.

摘要

雌性蚊子需要脊椎动物的血液来产卵，因此它们成为了毁灭性人类疾病的传播媒介。氨基酸 (AAs) 和营养物质来源于血食，激活卵黄生成并为自育蚊子的胚胎发育提供燃料。胰岛素样肽 (ILPs) 在雌性蚊子的繁殖中是不可或缺的，它们调节糖原和脂质代谢以及其他重要功能。然而，ILPs 如何协调其作用以响应蚊子繁殖中的 AA 涌入尚不清楚。我们在这里报告说，AA/雷帕霉素靶蛋白 (TOR) 信号通路通过 GATA 转录因子 (TF) 调节 ILPs。AA 输注结合 RNA 干扰 TOR 沉默揭示了它们在雌性蚊子中对 ILPs 的不同作用，即升高几种 ILPs 的循环水平，但抑制其他 ILPs 的水平，在雌性蚊子中。涉及同工型特异性 CRISPR-Cas9 基因组编辑和染色质免疫沉淀测定的实验表明，在低 AA-TOR 信号下，GATA 抑制因子 (GATAr) 同工型抑制 、 和 基因的表达，而在血食后，GATA 激活因子同工型激活 、 、 、 和 基因的表达，以响应增加的 AA-TOR 信号。FoxO，胰岛素途径中的下游 TF，参与了 TOR-GATAr 介导的 、 和 基因的抑制。这项工作揭示了 AA/TOR 信号如何控制 ILP 途径，以调节繁殖雌性蚊子的代谢需求。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/84be5049ee58/pnas.2303234120fig09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/d0ddda137de7/pnas.2303234120fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/7674c57098a1/pnas.2303234120fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/9917b31d7f34/pnas.2303234120fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/33ad01d88158/pnas.2303234120fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/49a9368702f7/pnas.2303234120fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/3503aa7c1d94/pnas.2303234120fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/77d07ffab11e/pnas.2303234120fig07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/b9520807c40e/pnas.2303234120fig08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/84be5049ee58/pnas.2303234120fig09.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/d0ddda137de7/pnas.2303234120fig01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/7674c57098a1/pnas.2303234120fig02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/9917b31d7f34/pnas.2303234120fig03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/33ad01d88158/pnas.2303234120fig04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/49a9368702f7/pnas.2303234120fig05.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/3503aa7c1d94/pnas.2303234120fig06.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/77d07ffab11e/pnas.2303234120fig07.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/b9520807c40e/pnas.2303234120fig08.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c45b/10450652/84be5049ee58/pnas.2303234120fig09.jpg

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