Exogenous siRNA mediates sequence-independent gene suppression by signaling through toll-like receptor 3

Cells Tissues Organs. 2004;177(3):132-8. doi: 10.1159/000079987.

Abstract

RNA interference (RNAi) is a powerful method that specifically suppresses gene expression in a sequence-dependent manner whose machinery is found in organisms from fungi to mammals. Mammalian cells have developed a sequence-independent system of gene suppression often induced by viral replication that includes the recognition of double-stranded RNA (dsRNA) through Toll-like receptor 3 (TLR3) and induction of type I interferon synthesis. Interferon activates the transcription of a set of genes including dsRNA-activated protein kinase that suppresses protein synthesis and 2'-5'-oligoadenylate synthetase, which generates a product that activates RNase L to cleave RNA in a sequence-independent manner. We observed that 21-bp dsRNA, a key mediator of RNAi, not only induces sequence-specific gene suppression, but also signals TLR3 to induce type I interferon and activates sequence-independent suppression of protein synthesis and enhancement of mRNA degradation. This sequence-independent suppression was demonstrated for both an exogenously administered reporter gene as well as during the targeting of viral genes in the course of acute herpes simplex virus type I infection of keratinocytes. As TLR3 is expressed by many primary cell types and cell lines, this sequence-independent suppression should be considered in the design of experiments using small interfering RNA-mediated gene suppression.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Cell Line
  • Genes, Reporter
  • Herpesvirus 1, Human / immunology
  • Herpesvirus 1, Human / pathogenicity
  • Humans
  • Luciferases / genetics
  • Membrane Glycoproteins / antagonists & inhibitors
  • Membrane Glycoproteins / genetics*
  • RNA Interference
  • RNA, Double-Stranded / genetics
  • RNA, Small Interfering / genetics*
  • Receptors, Cell Surface / antagonists & inhibitors
  • Receptors, Cell Surface / genetics*
  • Signal Transduction
  • Suppression, Genetic
  • Toll-Like Receptor 3
  • Toll-Like Receptors

Substances

  • Membrane Glycoproteins
  • RNA, Double-Stranded
  • RNA, Small Interfering
  • Receptors, Cell Surface
  • TLR3 protein, human
  • Toll-Like Receptor 3
  • Toll-Like Receptors
  • Luciferases