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Vol. 16, No. 19, pp. 2497-2508, October 1, 2002
1 Institute for Genome Research, 2 Graduate School
of Nutrition University of Tokushima, Tokushima 770-8503, Japan
Fragile X syndrome is a common form of inherited mental retardation
caused by the loss of FMR1 expression. The FMR1 gene
encodes an RNA-binding protein that associates with translating
ribosomes and acts as a negative translational regulator. In
Drosophila, the fly homolog of the FMR1 protein (dFMR1) binds
to and represses the translation of an mRNA encoding of the
microtuble-associated protein Futsch. We have isolated a
dFMR1-associated complex that includes two ribosomal proteins, L5 and
L11, along with 5S RNA. The dFMR1 complex also contains Argonaute2
(AGO2) and a Drosophila homolog of p68 RNA helicase (Dmp68).
AGO2 is an essential component for the RNA-induced silencing complex
(RISC), a sequence-specific nuclease complex that mediates RNA
interference (RNAi) in Drosophila. We show that Dmp68 is also
required for efficient RNAi. We further show that dFMR1 is associated
with Dicer, another essential component of the RNAi pathway, and
microRNAs (miRNAs) in vivo, suggesting that dFMR1 is part of the
RNAi-related apparatus. Our findings suggest a model in which the RNAi
and dFMR1-mediated translational control pathways intersect in
Drosophila. Our findings also raise the possibility that
defects in an RNAi-related machinery may cause human disease.
[Key Words: fragile X syndrome; FMR1; RNAi; RNA helicase; miRNA]
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