mut-7 of C-elegans, required for transposon silencing and RNA interference, is a homolog of Werner syndrome helicase and RNaseD

While all known natural isolates of C. elegans contain multiple copies of t he Tc1 transposon, which are active in the soma, Tc1 transposition is fully silenced in the germline of many strains. We mutagenized one such silenced strain and isolated mutants in which Tct had been activated in the germlin e ("mutators"). Interestingly, many other transposons of unrelated sequence had also become active. Most of these mutants are resistant to RNA interfe rence (RNAi). We found one of the mutated genes, mut-7, to encode a protein with homology to RNaseD. This provides support for the notion that RNAi wo rks by dsRNA-directed, enzymatic RNA degradation. We propose a model in whi ch MUT-7, guided by transposon-derived dsRNA, represses transposition by de grading transposon-specific messengers, thus preventing transposase product ion and transposition.