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Enhanced neuronal RNAi in C. elegans using SID-1.

We expressed SID-1, a transmembrane protein from Caenorhabditis elegans that is required for systemic RNA interference (RNAi), in C. elegans neurons. This expression increased the response of neurons to double-stranded (ds)RNA delivered by feeding. Mutations in the lin-15b and lin-35 genes enhanced this effect. Worms expressing neuronal SID-1 showed RNAi phenotypes when fed with bacteria expressing dsRNA for known neuronal genes and for uncharacterized genes with no previously known neuronal phenotypes. Neuronal expression of sid-1 decreased nonneuronal RNAi, suggesting that neurons expressing transgenic sid-1(+) served as a sink for dsRNA. This effect, or a sid-1(-) background, can be used to uncover neuronal defects for lethal genes. Expression of sid-1(+) from cell-specific promoters in sid-1 mutants results in cell-specific feeding RNAi. We used these strains to identify a role for integrin signaling genes in mechanosensation.

Pubmed ID: 20512143


  • Calixto A
  • Chelur D
  • Topalidou I
  • Chen X
  • Chalfie M


Nature methods

Publication Data

July 30, 2010

Associated Grants

  • Agency: NIGMS NIH HHS, Id: GM30997
  • Agency: NIGMS NIH HHS, Id: R37 GM030997
  • Agency: NIGMS NIH HHS, Id: R37 GM030997-25
  • Agency: NIGMS NIH HHS, Id: R37 GM030997-26
  • Agency: NIGMS NIH HHS, Id: R37 GM030997-27
  • Agency: NIGMS NIH HHS, Id: R37 GM030997-27S1

Mesh Terms

  • Animals
  • Caenorhabditis elegans
  • Caenorhabditis elegans Proteins
  • Gene Expression Regulation
  • Genes, Lethal
  • Membrane Proteins
  • Neurons
  • RNA Interference
  • Repressor Proteins
  • Transcription Factors