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miR-2703 通过靶向褐飞虱几丁质合酶 1a 调控几丁质生物合成途径。

miR-2703 regulates the chitin biosynthesis pathway by targeting chitin synthase 1a in Nilaparvata lugens.

机构信息

State Key Laboratory of Biocontrol, School of Life Sciences, Sun Yat-sen University, Guangzhou, Guangdong, China.

出版信息

Insect Mol Biol. 2020 Feb;29(1):38-47. doi: 10.1111/imb.12606. Epub 2019 Jul 17.

Abstract

The chitin biosynthesis pathway is an important physiology process in arthropods. However, few microRNAs (miRNAs) involved in the regulation of the chitin biosynthesis pathway in insects have been reported until now. In this study, four groups of samples that either upregulated or downregulated the chitin biosynthesis pathway were collected for deep sequencing, and a total of 15 unique mature miRNAs with significantly different expression levels were found, including 11 known miRNAs and four novel miRNAs. Subsequently, we showed that miR-2703 and its new target gene chitin synthase 1a are important for ecdysone-induced chitin biosynthesis in Nilaparvata lugens, a serious insect pest of rice. The nymphs showed an obvious moulting defect phenotype, lower survival rate and significantly reduced chitin content after miR-2703 feeding or injection. Furthermore, we found that the transcription level of miR-2703 was not repressed by 20-hydroxyecdysone signalling after Broad-Complex (BR-C) double-stranded RNA (dsRNA) injection compared with the repressed levels after green fluorescent protein dsRNA injection, suggesting that the involvement of miR-2703 in the 20-hydroxyecdysone pathway contributes to BR-C activity. miR-2703 regulates the chitin biosynthesis pathway by targeting chitin synthase 1a in response to 20-hydroxyecdysone signalling.

摘要

甲壳质生物合成途径是节肢动物的重要生理过程。然而,到目前为止,在昆虫中只有少数 microRNAs(miRNAs)参与调控甲壳质生物合成途径。在这项研究中,收集了上调或下调甲壳质生物合成途径的四组样本进行深度测序,共发现了 15 个具有显著差异表达水平的独特成熟 miRNA,包括 11 个已知的 miRNA 和 4 个新的 miRNA。随后,我们表明,miR-2703 及其新的靶基因 chitin synthase 1a 在褐飞虱 Nilaparvata lugens 蜕皮激素诱导的甲壳质生物合成中起重要作用,褐飞虱是水稻的一种严重害虫。miR-2703 喂食或注射后,若虫表现出明显的蜕皮缺陷表型、存活率降低和甲壳质含量显著降低。此外,我们发现与绿色荧光蛋白 dsRNA 注射后的抑制水平相比,在 Broad-Complex(BR-C)双链 RNA(dsRNA)注射后,20-羟基蜕皮酮信号没有抑制 miR-2703 的转录水平,这表明 miR-2703 参与 20-羟基蜕皮酮途径有助于 BR-C 活性。miR-2703 通过靶向 chitin synthase 1a 来调节甲壳质生物合成途径,以响应 20-羟基蜕皮酮信号。

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