生物谷援引華文生技網(wǎng)報(bào)道：微型RNA (MicroRNAs,；簡(jiǎn)稱miRNA) 的發(fā)現(xiàn)，是細(xì)胞研究上重要的發(fā)現(xiàn),，因?yàn)榫头肿由飳W(xué)的中心法則 (central dogma)來(lái)說(shuō),，含有遺傳信息的 DNA，通過(guò)轉(zhuǎn)錄(transcription) 形成信使RNA(messenger RNAs) ,，再經(jīng)由翻譯(translation) 產(chǎn)生蛋白質(zhì),，這個(gè)過(guò)程中miRNA 雖然影響了30% 的基因活動(dòng)，但科學(xué)家對(duì)于它真正的作用機(jī)制,，卻仍然不是那么清楚,。最近由歐洲分子生物學(xué)實(shí)驗(yàn)室(European Molecular Biology Laboratory ；簡(jiǎn)稱EMBL)的科學(xué)家,，發(fā)表在最新一期自然 (Nature)期刊的一篇論文,，通過(guò)一種新的技術(shù)，可以在體外清楚的觀察到 miRNA的作用全過(guò)程,，可以說(shuō)將 miRNA的研究,，帶進(jìn)了一個(gè)嶄新的領(lǐng)域。
EMBL 實(shí)驗(yàn)到的Rolf Thermann博士所主持的實(shí)驗(yàn)計(jì)劃,，利用果蠅 (fruitfly)胚胎這個(gè)極易觀察的動(dòng)物模型,，嘗試著分析 miRNA的運(yùn)作過(guò)程，結(jié)果研究人員發(fā)現(xiàn)了一個(gè)稱為 miR2的微型核糖核酸,，在果蠅的生長(zhǎng)發(fā)育過(guò)程中,，參與很多的過(guò)程，而很特別的是研究人員發(fā)現(xiàn)當(dāng)這個(gè) miRNA的分子粘上mRNA 時(shí)候,，就像是mRNA 與核糖體(ribosome)組合,，即將進(jìn)行翻譯的動(dòng)作，但實(shí)際上并沒(méi)有任何的蛋白質(zhì)生成,。
科學(xué)家認(rèn)為 miRNA活動(dòng)過(guò)程的方式,，并沒(méi)有因?yàn)橐浦驳襟w外而有所改變,，因此使得這種直接在體外觀察的方式，成了 miRNA研究的新平臺(tái),，將來(lái)與 miRNA相關(guān)的研究，甚至直接跟疾病相關(guān)的 miRNA,，都有可能因此揭開(kāi)了神秘的面紗,。
(資料來(lái)源 : biocompare)
英文原文鏈接：
http://news.biocompare.com/newsstory.asp?id=183071
原始出處：
Letter
Nature advance online publication 16 May 2007 | doi:10.1038/nature05878; Received 7 November 2006; Accepted 26 April 2007; Published online 16 May 2007
Drosophila miR2 induces pseudo-polysomes and inhibits translation initiation
Rolf Thermann1 & Matthias W. Hentze1
European Molecular Biology Laboratory, Meyerhofstrasse 1, D-69117 Heidelberg, Germany
Correspondence to: Matthias W. Hentze1 Correspondence and requests for materials should be addressed to M.W.H. (Email: [email protected]).
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MicroRNAs (miRs) inhibit protein synthesis by mechanisms that are as yet unresolved1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11. We developed a cell-free system from Drosophila melanogaster embryos that faithfully recapitulates miR2-mediated translational control by means of the 3' untranslated region of the D. melanogaster reaper messenger RNA. Here we show that miR2 inhibits translation initiation without affecting mRNA stability. Surprisingly, miR2 induces the formation of dense (heavier than 80S) miRNPs ('pseudo-polysomes') even when polyribosome formation and 60S ribosomal subunit joining are blocked. An mRNA bearing an ApppG instead of an m7GpppG cap structure escapes the miR2-mediated translational block. These results directly show the inhibition of m7GpppG cap-mediated translation initiation as the mechanism of miR2 function, and uncover pseudo-polysomal messenger ribonucleoprotein assemblies that may help to explain earlier findings.
