上游开放阅读框抑制了 iab-8 RNA 的翻译。

IF 4 2区 生物学 Q1 GENETICS & HEREDITY
PLoS Genetics Pub Date : 2024-09-23 eCollection Date: 2024-09-01 DOI:10.1371/journal.pgen.1011214
Yohan Frei, Clément Immarigeon, Maxime Revel, François Karch, Robert K Maeda
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引用次数: 0

摘要

尽管最初被归类为非编码 RNA,但最近研究表明,来自黑腹果蝇双顶复合体的雄性特异性腹部(MSA)RNA编码一种微肽,这种微肽在决定交配后雌性如何使用储存的精子方面起着至关重要的作用。有趣的是,MSA 转录本是另一种转录本的雄性特异性版本,另一种转录本产生于雌雄后部中枢神经系统中的另一个启动子,称为 iab-8 lncRNA。然而,MSA 转录本能产生一种小肽,而 iab-8 转录本似乎不能。在这里,我们证明 iab-8 翻译的缺失是由于一种需要 iab-8 lncRNA 的两个独特的 5' 外显子的抑制机制造成的。通过细胞培养和转基因分析,我们表明这种机制依赖于这两个外显子中存在的上游开放阅读框,它们阻止了下游开放阅读框产生蛋白质。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Upstream open reading frames repress the translation from the iab-8 RNA.

Although originally classified as a non-coding RNA, the male-specific abdominal (MSA) RNA from the Drosophila melanogaster bithorax complex has recently been shown to code for a micropeptide that plays a vital role in determining how mated females use stored sperm after mating. Interestingly, the MSA transcript is a male-specific version of another transcript produced in both sexes within the posterior central nervous system from an alternative promoter, called the iab-8 lncRNA. However, while the MSA transcript produces a small peptide, it seems that the iab-8 transcript does not. Here, we show that the absence of iab-8 translation is due to a repressive mechanism requiring the two unique 5' exons of the iab-8 lncRNA. Through cell culture and transgenic analysis, we show that this mechanism relies on the presence of upstream open reading frames present in these two exons that prevent the production of proteins from downstream open reading frames.

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来源期刊
PLoS Genetics
PLoS Genetics GENETICS & HEREDITY-
自引率
2.20%
发文量
438
期刊介绍: PLOS Genetics is run by an international Editorial Board, headed by the Editors-in-Chief, Greg Barsh (HudsonAlpha Institute of Biotechnology, and Stanford University School of Medicine) and Greg Copenhaver (The University of North Carolina at Chapel Hill). Articles published in PLOS Genetics are archived in PubMed Central and cited in PubMed.
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