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

Cell. 1999 Oct 15;99(2):133-41. doi: 10.1016/s0092-8674(00)81645-1.


While all known natural isolates of C. elegans contain multiple copies of the 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 Tc1 had been activated in the germline ("mutators"). Interestingly, many other transposons of unrelated sequence had also become active. Most of these mutants are resistant to RNA interference (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 works by dsRNA-directed, enzymatic RNA degradation. We propose a model in which MUT-7, guided by transposon-derived dsRNA, represses transposition by degrading transposon-specific messengers, thus preventing transposase production and transposition.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Caenorhabditis elegans / genetics*
  • Caenorhabditis elegans / metabolism*
  • DNA Helicases / chemistry*
  • DNA Helicases / genetics
  • DNA Transposable Elements*
  • Endoribonucleases / chemistry*
  • Endoribonucleases / genetics
  • Humans
  • Models, Genetic
  • Molecular Sequence Data
  • Mutagenesis, Insertional
  • Polymerase Chain Reaction
  • RNA, Double-Stranded / genetics
  • RNA, Helminth / genetics
  • RNA, Messenger / genetics
  • Recombinant Proteins / chemistry
  • Ribonuclease III
  • Sequence Alignment
  • Sequence Homology, Amino Acid
  • Werner Syndrome / enzymology
  • Werner Syndrome / genetics*


  • DNA Transposable Elements
  • RNA, Double-Stranded
  • RNA, Helminth
  • RNA, Messenger
  • Recombinant Proteins
  • Endoribonucleases
  • Ribonuclease III
  • DNA Helicases