| Autor: |
Thivierge C; Department of Biochemistry, McGill University, Montreal, Quebec, Canada., Makil N, Flamand M, Vasale JJ, Mello CC, Wohlschlegel J, Conte D Jr, Duchaine TF |
| Jazyk: |
angličtina |
| Zdroj: |
Nature structural & molecular biology [Nat Struct Mol Biol] 2011 Dec 18; Vol. 19 (1), pp. 90-7. Date of Electronic Publication: 2011 Dec 18. |
| DOI: |
10.1038/nsmb.2186 |
| Abstrakt: |
Endogenous RNA interference (endo-RNAi) pathways use a variety of mechanisms to generate siRNA and to mediate gene silencing. In Caenorhabditis elegans, DCR-1 is essential for competing RNAi pathways-the ERI endo-RNAi pathway and the exogenous RNAi pathway-to function. Here, we demonstrate that DCR-1 forms exclusive complexes in each pathway and further define the ERI-DCR-1 complex. We show that the tandem tudor protein ERI-5 potentiates ERI endo-RNAi by tethering an RNA-dependent RNA polymerase (RdRP) module to DCR-1. In the absence of ERI-5, the RdRP module is uncoupled from DCR-1. Notably, EKL-1, an ERI-5 paralog that specifies distinct RdRP modules in Dicer-independent endo-RNAi pathways, partially compensates for the loss of ERI-5 without interacting with DCR-1. Our results implicate tudor proteins in the recruitment of RdRP complexes to specific steps within DCR-1-dependent and DCR-1-independent endo-RNAi pathways. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
|
