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本文引用的文献

1
Chronologically inappropriate morphogenesis () is required for maintenance of larval stages of fall armyworm.胚胎形态发生的时间异常是秋黏虫幼虫期得以维持的必要条件。
Proc Natl Acad Sci U S A. 2024 Dec 3;121(49):e2411286121. doi: 10.1073/pnas.2411286121. Epub 2024 Nov 26.
2
Determination of Key Components in the p53 Apoptosis Regulation Network Using Y2H-Seq.使用酵母双杂交测序法确定p53凋亡调控网络中的关键成分
Insects. 2023 Apr 5;14(4):362. doi: 10.3390/insects14040362.
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Reduction of embryonic expression as a hypothetical driver of the evolution of insect metamorphosis.胚胎表达减少假说作为昆虫变态进化的驱动力。
Proc Natl Acad Sci U S A. 2023 Feb 14;120(7):e2216640120. doi: 10.1073/pnas.2216640120. Epub 2023 Feb 6.
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Mitochondria dysfunction impairs Tribolium castaneum wing development during metamorphosis.线粒体功能障碍会影响三化螟在变态过程中翅膀的发育。
Commun Biol. 2022 Nov 15;5(1):1252. doi: 10.1038/s42003-022-04185-z.
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CRISPR-Cas9 Genome Editing Uncovers the Mode of Action of Methoprene in the Yellow Fever Mosquito, .CRISPR-Cas9 基因组编辑揭示了保幼激素在黄热病蚊中的作用模式。
CRISPR J. 2022 Dec;5(6):813-824. doi: 10.1089/crispr.2022.0066. Epub 2022 Nov 14.
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The TGF-β Receptor Gene Influences Larval-Pupal-Adult Development in .TGF-β 受体基因影响 的幼虫-蛹-成虫发育。
Molecules. 2022 Sep 15;27(18):6017. doi: 10.3390/molecules27186017.
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KMT5A-methylated SNIP1 promotes triple-negative breast cancer metastasis by activating YAP signaling.KMT5A 甲基化的 SNIP1 通过激活 YAP 信号促进三阴性乳腺癌转移。
Nat Commun. 2022 Apr 21;13(1):2192. doi: 10.1038/s41467-022-29899-w.
8
Distinct developmental phenotypes result from mutation of Set8/KMT5A and histone H4 lysine 20 in Drosophila melanogaster.Set8/KMT5A 和组蛋白 H4 赖氨酸 20 的突变导致果蝇出现不同的发育表型。
Genetics. 2022 May 31;221(2). doi: 10.1093/genetics/iyac054.
9
is the larval member of the molecular trinity that directs metamorphosis.是分子三位一体的幼虫成员,指导变态。
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10
Juvenile hormone-induced histone deacetylase 3 suppresses apoptosis to maintain larval midgut in the yellow fever mosquito.保幼激素诱导的组蛋白去乙酰化酶 3 抑制细胞凋亡以维持黄热病蚊幼虫中肠。
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组蛋白甲基化在昆虫发育中的作用:KMT5A在赤拟谷盗变态过程中调节蜕皮甾体生物合成。

Role of histone methylation in insect development: KMT5A regulates ecdysteroid biosynthesis during metamorphosis of Tribolium castaneum.

作者信息

Jiao Yaoyu, Sengodan Karthi, Chen Jiasheng, Palli Subba Reddy

机构信息

Department of Entomology, Martin-Gatton College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY, 40546, USA.

Department of Entomology, Martin-Gatton College of Agriculture, Food and Environment, University of Kentucky, Lexington, KY, 40546, USA.

出版信息

Insect Biochem Mol Biol. 2025 May;180:104316. doi: 10.1016/j.ibmb.2025.104316. Epub 2025 Apr 24.

DOI:10.1016/j.ibmb.2025.104316
PMID:40287070
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12066215/
Abstract

Methylation levels of core histones play important roles in the regulation of gene expression and impact animal development. However, the methyltransferases and demethylases that determine histone methylation levels remain largely unexplored in insects. Most of our current understanding of histone methylation comes from mammalian studies. In this study, we first identified potential histone methyltransferases and demethylases encoded in the genome of the red flour beetle Tribolium castaneum. The function of these histone methylation enzymes in the metamorphosis was investigated by knocking down genes coding for these enzymes using RNA interference (RNAi). Our results showed that a lysine methyltransferase, KMT5A, plays a critical role in T. castaneum metamorphosis by regulating the biosynthesis of ecdysteroids. Treating KMT5A-knockdown larvae with 20 hydroxyecdysone can partially rescue T. castaneum pupation. Western blot analysis showed that KMT5A catalyzes H4K20 mono-methylation. However, further studies suggest that KMT5A may regulate T. castaneum pupation through mechanisms independent of H4K20 methylation. These data uncovered the roles of histone methylation enzymes in T. castaneum metamorphosis and KMT5A as a critical regulator of ecdysteroid biosynthesis.

摘要

核心组蛋白的甲基化水平在基因表达调控和影响动物发育过程中发挥着重要作用。然而,在昆虫中,决定组蛋白甲基化水平的甲基转移酶和去甲基化酶在很大程度上仍未被探索。我们目前对组蛋白甲基化的大多数了解来自哺乳动物研究。在本研究中,我们首先在赤拟谷盗(Tribolium castaneum)的基因组中鉴定出潜在的组蛋白甲基转移酶和去甲基化酶。通过使用RNA干扰(RNAi)敲低编码这些酶的基因,研究了这些组蛋白甲基化酶在变态过程中的功能。我们的结果表明,一种赖氨酸甲基转移酶KMT5A通过调节蜕皮激素的生物合成,在赤拟谷盗的变态过程中发挥关键作用。用20-羟基蜕皮酮处理KMT5A敲低的幼虫可以部分挽救赤拟谷盗的化蛹。蛋白质免疫印迹分析表明,KMT5A催化H4K20单甲基化。然而,进一步的研究表明,KMT5A可能通过独立于H4K20甲基化的机制调节赤拟谷盗的化蛹。这些数据揭示了组蛋白甲基化酶在赤拟谷盗变态过程中的作用以及KMT5A作为蜕皮激素生物合成的关键调节因子的作用。