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PGE 通过 cAMP 信号通路上调鳞翅目昆虫中肠双氧化酶的基因表达。

PGE upregulates gene expression of dual oxidase in a lepidopteran insect midgut via cAMP signalling pathway.

机构信息

Department of Plant Medicals, College of Life Sciences, Andong National University, Andong 36729, Korea.

出版信息

Open Biol. 2020 Oct;10(10):200197. doi: 10.1098/rsob.200197. Epub 2020 Oct 21.

DOI:10.1098/rsob.200197
PMID:33081632
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7653354/
Abstract

In insect midgut, prostaglandins (PGs) play a crucial role in defending bacterial and malarial pathogens. However, little is known about the PG signalling pathway in the midgut. A dual oxidase () with presumed function of catalysing reactive oxygen species (ROS) production in the midgut was identified in beet armyworm, . was expressed in all developmental stages, exhibiting relatively high expression levels in the midgut of late larval instars. expression was upregulated upon bacterial challenge. RNA interference (RNAi) of expression significantly suppressed ROS levels in the midgut lumen. The suppression of ROS levels increased insecticidal activity of after oral infection. Interestingly, treatment with a PLA inhibitor prevented the induction of expression in response to bacterial challenge. On the other hand, addition of its catalytic product rescued the induction of expression. Especially, PG synthesis inhibitor significantly suppressed expression, while the addition of PGE or PGD rescued the inhibition. Subsequent PG signals involved cAMP and downstream components because specific inhibitors of cAMP signal components such as adenylate cyclase (AC) and protein kinase A (PKA) significantly inhibited expression. Indeed, addition of a cAMP analogue stimulated expression in the midgut. Furthermore, individual RNAi specific to PGE receptor (a trimeric G-protein subunit), AC, PKA or cAMP-responsive element-binding protein resulted in suppression of expression. These results suggest that PGs can activate midgut immunity via cAMP signalling pathway by inducing expression along with increased ROS levels.

摘要

在昆虫的中肠中,前列腺素 (PGs) 在抵御细菌和疟原虫病原体方面发挥着关键作用。然而,人们对中肠中的 PG 信号通路知之甚少。在甜菜夜蛾 中鉴定出一种具有催化中肠活性氧 (ROS) 产生的假定功能的双氧化酶 ()。 在所有发育阶段都有表达,在后期幼虫期的中肠中表达水平相对较高。 表达在受到细菌挑战时上调。 表达的 RNA 干扰 (RNAi) 显著抑制了中肠腔中的 ROS 水平。抑制 ROS 水平后, 经口服感染后的杀虫活性增加。有趣的是,用 PLA 抑制剂处理可防止 ROS 水平因细菌挑战而升高。另一方面,其催化产物的添加挽救了 表达的诱导。特别是,PG 合成抑制剂显著抑制 表达,而 PGE 或 PGD 的添加则挽救了抑制。随后的 PG 信号涉及 cAMP 和下游成分,因为 cAMP 信号成分(如腺苷酸环化酶 (AC) 和蛋白激酶 A (PKA))的特定抑制剂显著抑制 表达。事实上,添加 cAMP 类似物可刺激中肠 表达。此外,针对 PGE 受体(三聚体 G 蛋白亚基)、AC、PKA 或 cAMP 反应元件结合蛋白的特定 RNAi 也抑制了 表达。这些结果表明,PG 可以通过诱导 表达和增加 ROS 水平来激活中肠免疫,从而激活 cAMP 信号通路。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/c1be096668ba/rsob-10-200197-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/eda161154593/rsob-10-200197-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/3da352dc506b/rsob-10-200197-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/ee270e582dce/rsob-10-200197-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/ce66d8b00955/rsob-10-200197-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/af568ba0e02e/rsob-10-200197-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/c2ee5e378637/rsob-10-200197-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/c1be096668ba/rsob-10-200197-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/eda161154593/rsob-10-200197-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/3da352dc506b/rsob-10-200197-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/ee270e582dce/rsob-10-200197-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/ce66d8b00955/rsob-10-200197-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/af568ba0e02e/rsob-10-200197-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/c2ee5e378637/rsob-10-200197-g6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0d67/7653354/c1be096668ba/rsob-10-200197-g7.jpg

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