Abstract
To address the biological function of RNA interference (RNAi)-related pathways in mammals, we disrupted the gene Dicer1 in mice. Loss of Dicer1 lead to lethality early in development, with Dicer1-null embryos depleted of stem cells. Coupled with our inability to generate viable Dicer1-null embryonic stem (ES) cells, this suggests a role for Dicer, and, by implication, the RNAi machinery, in maintaining the stem cell population during early mouse development.
Publication types
- Research Support, Non-U.S. Gov't
- Research Support, U.S. Gov't, Non-P.H.S.
- Research Support, U.S. Gov't, P.H.S.
MeSH terms
- Amino Acid Sequence
- Animals
- DEAD-box RNA Helicases
- Embryonic and Fetal Development / physiology*
- Endoribonucleases / genetics
- Endoribonucleases / physiology*
- Mice
- Mice, Knockout
- Molecular Sequence Data
- RNA Helicases / genetics
- RNA Helicases / physiology*
- RNA Interference
- Ribonuclease III
- Stem Cells / cytology
Substances
- Endoribonucleases
- DICER1 protein, human
- Ribonuclease III
- DEAD-box RNA Helicases
- RNA Helicases