真核生物已經(jīng)進化出了復雜的機制，通過蛋白感受器,、傳感器及作用因子的協(xié)同作用來進行DNA雙鏈斷裂修復(DSBs),。
北京生命科學研究所的戚益軍等人研究發(fā)現(xiàn)，在擬南芥及人類細胞中,，DSB位點附近產(chǎn)生了大小約21個核苷酸的小RNAs,。研究人員把這些小RNAs稱作對DSB誘導的小RNAs有關(guān)的diRNAs。相關(guān)論文發(fā)表在3月30日的Cell,。
在擬南芥中,，diRNAs的產(chǎn)生需要PI3激酶ATR,，RNA合成酶IV(Pol IV)，以及Dicer樣蛋白,。這些蛋白及Pol V的突變會引起DSB修復效率顯著的降低,。
而且，在擬南芥中,，diRNAs是由Argonaute蛋白2(AGO2)招募來介導DSB的修復,。在人類細胞中，敲除Dicer或Ago2同樣會降低DSB的修復效率,。
研究結(jié)果表明,，diRNAs介導的DSB修復在人類及植物中是保守的。
因此,，diRNAs很能是作為一個引導分子來指向染色體修飾,，或者是招募蛋白復合體到DSB位點來幫助修復。（生物谷Deepblue編譯）
doi: 10.1016/j.cell.2012.03.002
PMC:
PMID:
A Role for Small RNAs in DNA Double-Strand Break Repair
Wei Wei, Zhaoqing Ba, Min Gao, Yang Wu, Yanting Ma, Simon Amiard, Charles I. White, Jannie Michaela Rendtlew Danielsen, Yun-Gui Yang, Yijun Qi .
Eukaryotes have evolved complex mechanisms to repair DNA double-strand breaks (DSBs) through coordinated actions of protein sensors, transducers, and effectors.Here we show that ～21-nucleotide small RNAs are produced from the sequences in the vicinity of DSB sites in Arabidopsis and in human cells. We refer to these as diRNAs for DSB-induced small RNAs.In Arabidopsis, the biogenesis of diRNAs requires the PI3 kinase ATR, RNA polymerase IV (Pol IV), and Dicer-like proteins. Mutations in these proteins as well as in Pol V cause significant reduction in DSB repair efficiency.In Arabidopsis, diRNAs are recruited by Argonaute 2 (AGO2) to mediate DSB repair. Knock down of Dicer or Ago2 in human cells reduces DSB repair.Our findings reveal a conserved function for small RNAs in the DSB repair pathway.We propose that diRNAs may function as guide molecules directing chro.
