Liu Jidong, Rivas Fabiola V, Wohlschlegel James, Yates John R, Parker Roy, Hannon Gregory J
Cold Spring Harbor Laboratory, Watson School of Biological Sciences, Howard Hughes Medical Institute, 1 Bungtown Road, Cold Spring Harbor, NY 11724, USA.
Nat Cell Biol. 2005 Dec;7(12):1261-6. doi: 10.1038/ncb1333. Epub 2005 Nov 13.
In animals, the majority of microRNAs regulate gene expression through the RNA interference (RNAi) machinery without inducing small-interfering RNA (siRNA)-directed mRNA cleavage. Thus, the mechanisms by which microRNAs repress their targets have remained elusive. Recently, Argonaute proteins, which are key RNAi effector components, and their target mRNAs were shown to localize to cytoplasmic foci known as P-bodies or GW-bodies. Here, we show that the Argonaute proteins physically interact with a key P-/GW-body subunit, GW182. Silencing of GW182 delocalizes resident P-/GW-body proteins and impairs the silencing of microRNA reporters. Moreover, mutations that prevent Argonaute proteins from localizing in P-/GW-bodies prevent translational repression of mRNAs even when Argonaute is tethered to its target in a siRNA-independent fashion. Thus, our results support a functional link between cytoplasmic P-bodies and the ability of a microRNA to repress expression of a target mRNA.
在动物中,大多数微小RNA通过RNA干扰(RNAi)机制调节基因表达,而不会诱导小干扰RNA(siRNA)介导的mRNA切割。因此,微小RNA抑制其靶标的机制仍然不清楚。最近,作为关键RNAi效应成分的AGO蛋白及其靶标mRNA被证明定位于称为P小体或GW小体的细胞质焦点。在这里,我们表明AGO蛋白与关键的P-/GW-体亚基GW182发生物理相互作用。GW182的沉默使驻留的P-/GW-体蛋白发生异位,并损害微小RNA报告基因的沉默。此外,阻止AGO蛋白定位于P-/GW-体的突变会阻止mRNA的翻译抑制,即使AGO以不依赖siRNA的方式与靶标相连。因此,我们的结果支持细胞质P小体与微小RNA抑制靶标mRNA表达能力之间的功能联系。