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
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Animals
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DEAD-box RNA Helicases
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Embryonic and Fetal Development / physiology*
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Endoribonucleases / genetics
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Endoribonucleases / physiology*
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Mice
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Mice, Knockout
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Molecular Sequence Data
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RNA Helicases / genetics
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RNA Helicases / physiology*
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RNA Interference
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Ribonuclease III
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Stem Cells / cytology
Substances
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Endoribonucleases
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DICER1 protein, human
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Ribonuclease III
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DEAD-box RNA Helicases
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RNA Helicases