CGC Bibliography Paper 5423

Loss of the putative RNA-directed RNA polymerase RRF-3 makes C. elegans hypersensitive to RNAi.

Simmer F, Tijsterman M, Parrish S, Koushika SP, Nonet ML, Fire A, Ahringer J, Plasterk RHA

Medline:

12176360

Citation:

Current Biology 12: 1317-1319 2002

Type:

ARTICLE

Genes:

apr-1 cel-1 clr-1 cye-1 daf-2 dpy-14 dpy-18 eft-3 egl-30 efr-1 gon-4 gpc-2 gsa-1 him-3 hlh-1 hmr-1 lag-2 let-502 lin-1 lin-31 lin-49 mom-5 mut-7 mut-16 par-1 pha-1 pop-1 pos-1 ptr-2 rde-4 rec-8 ric-19 rrf-3 spo-11 unc-3 unc-4 unc-5 und-6 unc-11 unc-12 unc-13 unc-14 unc-15 unc-17 unc-22 unc-29 unc-30 unc-33 unc-36 unc-37 unc-38 unc-40 unc-47 unc-73 unc-76 unc-86 unc-87 unc-89 unc-93 unc-101 unc-104 unc-130 zyg-1

Abstract:

RNA interference (RNAi) is a broadly used reverse genetics method in C. elegans [1]. Unfortunately, RNAi does not inhibit all genes [2,3]. We show that loss of function of a putative RNA-directed RNA polymerase (RdRP) of C. elegans, RRF-3, results in a substantial enhancement of sensitivity to RNAi in diverse tissues. This is particularly striking in the nervous system; neurons that are generally refractory to RNAi in a wild-type genetic background can respond effectively to interference in an rrf-3 mutant background. These data provide the first indication of physiological negative modulation of the RNAi response and implicate an RdRP-related factor in this effect. Therrf-3 strain can be useful to study genes that, in wild-type, do not show a phenotype after RNAi, and it is probably the strain of choice for genome-wide RNAi screens.