Loqs and R2D2 act sequentially in the siRNA pathway in Drosophila.

Loqs and R2D2 act sequentially in the siRNA pathway in Drosophila.
复制标题

DOI:
10.1038/nsmb.1735
复制
发表时间:
2010-01
影响因子:
16.8
通讯作者:
--
中科院分区:
生物学1区
文献类型:
--
作者:

文献摘要

参考文献

被引文献

相似文献

在黑腹果蝇中,小干扰RNA(siRNA)途径由外源性双链RNA(dsRNA)或在病毒感染时触发。该途径需要Dicer-2(Dcr-2)与称为R2D2的dsRNA结合蛋白(dsRBP)结合。一个潜在的独特的siRNA途径,需要Dcr-2与不同的dsRBP,称为Loquacious(Loqs),被激活的内源性dsRNA来自转座子,结构化基因座和重叠的转录本。在这里,我们表明,不同来源的dsRNA进入一个共同的siR-NA途径,需要R2D2和Loqs。R2D2和loqs突变体显示由外源dsRNA注射或内源dsRNA的人工和天然表达触发的受损沉默。此外,我们表明,这些dsRBP功能顺序和非冗余与Dcr-2的合作。Loqs主要是dsRNA加工所需的,而R2D2是随后将siRNA加载到效应物Ago-RISC复合物中所必需的。
In Drosophila melanogaster, the small interfering RNA (siRNA) pathway is triggered by exogenous double-stranded RNA (dsRNA) or upon viral infection. This pathway requires Dicer-2 (Dcr-2) in association with a dsRNA binding protein (dsRBP) called R2D2. A potentially distinct siRNA pathway, which requires Dcr-2 in association with a different dsRBP, called Loquacious (Loqs), is activated by endogenous dsRNA derived from transposons, structured loci and overlapping transcripts. Here, we show that different sources of dsRNA enter a common siR-NA pathway that requires R2D2 and Loqs. R2D2 and loqs mutants show impaired silencing triggered by injection of exogenous dsRNA or by artificial and natural expression of endogenous dsRNA. In addition, we show that these dsRBPs function sequentially and non-redundantly in collaboration with Dcr-2. Loqs is primarily required for dsRNA processing while R2D2 is essential for the subsequent loading of siRNAs into effector Ago-RISC complexes.
DOI: 10.1101/gad.1334005
发表时间: 2005-07-15
影响因子: 10.5
作者:
Jiang, F;Ye, XC;Liu, QH
通讯作者: Liu, QH
DOI: 10.1074/jbc.m611768200
发表时间: 2007-06-15
影响因子: 4.8
作者:
Kok, Kin Hang;Ng, Ming-Him James;Jin, Dong-Yan
通讯作者: Jin, Dong-Yan
DOI: 10.1016/j.cub.2007.01.060
发表时间: 2007-03-20
期刊: CURRENT BIOLOGY
影响因子: 9.2
作者:
Park, Joseph K.;Liu, Xiang;Liu, Qinghua
通讯作者: Liu, Qinghua
DOI: 10.1016/j.cub.2007.06.030
发表时间: 2007-07-17
期刊: CURRENT BIOLOGY
影响因子: 9.2
作者:
Horwich, Michael D.;Li, Chengjian;Zamore, Phillip D.
通讯作者: Zamore, Phillip D.
DOI: 10.1016/j.cell.2009.01.045
发表时间: 2009-02-20
期刊: Cell
影响因子: 64.5
作者:
Malone CD;Hannon GJ
通讯作者: Hannon GJ