| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 1937621 | Biochemical and Biophysical Research Communications | 2007 | 7 Pages |
RNA interference (RNAi), a post-transcriptional gene silencing mechanism originally described in Caenorhabditis elegans, involves sequence-specific mRNA degradation mediated by double-stranded RNAs (dsRNAs). Passive dsRNA uptake has been uniquely observed in C. elegans due to the expression of systemic RNA interference defective-1 (SID-1). Here we investigated the ability of ectopic SID-1 expression to enable passive cellular uptake of short interfering RNA (siRNA) or double stranded RNA (dsRNA) in pluripotent mouse embryonic stem cells (mESCs). When SID-1-GFP and the Firefly luciferase reporter gene (lucFir) were co-expressed in mESCs, lucFir activity could be suppressed by simple incubation with dsRNAs/siRNAs that were designed to specifically target lucFir. By contrast, suppression was not observed in mESCs expressing lucFir and GFP alone or when either GFP- or SID-1-GFP-expressing cells were incubated with control dsRNAs/siRNAs (non-silencing or Renilla luciferase-specific). These results may lead to high-throughput experimental strategies for studying ESC differentiation and novel approaches to genetically inhibit or eliminate the tumorigenicity of ESCs.
