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.
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Acknowledgements
We thank L. Bianco and J. Coblentz for assistance with animals; B. Holdener, M.J. Garcia-Garcia and the Stony Brook University Histology Facility for help with initial embryo dissections; and M. Zhang and Z. Xuan for bioinformatics. E.M. is a Elisabeth Sloane Livingston Fellow of the Watson School of Biological Sciences. M.C. is supported by a US Army Breast Cancer Research Program Predoctoral Fellowship. This work was supported in part by grants from the US National Institutes of Health (G.J.H, S.J.E. and K.V.A) and the Howard Hughes Medical Institute (S.J.E.).
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Bernstein, E., Kim, S., Carmell, M. et al. Dicer is essential for mouse development. Nat Genet 35, 215–217 (2003). https://doi.org/10.1038/ng1253
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DOI: https://doi.org/10.1038/ng1253
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