Dicer is essential for mouse development

Emily Bernstein; Sang Yong Kim; Michelle A. Carmell; Elizabeth P. Murchison; Heather Alcorn; Mamie Z. Li; Alea A. Mills; Stephen J. Elledge; Kathryn V. Anderson; Gregory J. Hannon

doi:10.1038/ng1253

Dicer is essential for mouse development

Emily Bernstein
, Sang Yong Kim
, Michelle A. Carmell
, Elizabeth P. Murchison
, Heather Alcorn
, Mamie Z. Li
, Alea A. Mills
, Stephen J. Elledge
, Kathryn V. Anderson
, Gregory J. Hannon

Research output: Contribution to journal › Article › peer-review

1692 Scopus citations

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.

Original language	English
Pages (from-to)	215-217
Number of pages	3
Journal	Nature Genetics
Volume	35
Issue number	3
DOIs	https://doi.org/10.1038/ng1253
State	Published - Nov 2003
Externally published	Yes

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10.1038/ng1253

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@article{36c6292f801f4a3d99770b3ea20970aa,

title = "Dicer is essential for mouse development",

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.",

author = "Emily Bernstein and Kim, \{Sang Yong\} and Carmell, \{Michelle A.\} and Murchison, \{Elizabeth P.\} and Heather Alcorn and Li, \{Mamie Z.\} and Mills, \{Alea A.\} and Elledge, \{Stephen J.\} and Anderson, \{Kathryn V.\} and Hannon, \{Gregory J.\}",

note = "Funding Information: 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.).",

year = "2003",

month = nov,

doi = "10.1038/ng1253",

language = "English",

volume = "35",

pages = "215--217",

journal = "Nature Genetics",

issn = "1061-4036",

publisher = "Nature Research",

number = "3",

}

TY - JOUR

T1 - Dicer is essential for mouse development

AU - Bernstein, Emily

AU - Kim, Sang Yong

AU - Carmell, Michelle A.

AU - Murchison, Elizabeth P.

AU - Alcorn, Heather

AU - Li, Mamie Z.

AU - Mills, Alea A.

AU - Elledge, Stephen J.

AU - Anderson, Kathryn V.

AU - Hannon, Gregory J.

N1 - Funding Information: 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.).

PY - 2003/11

Y1 - 2003/11

N2 - 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.

AB - 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.

UR - https://www.scopus.com/pages/publications/0242266620

U2 - 10.1038/ng1253

DO - 10.1038/ng1253

M3 - Article

C2 - 14528307

AN - SCOPUS:0242266620

SN - 1061-4036

VL - 35

SP - 215

EP - 217

JO - Nature Genetics

JF - Nature Genetics

IS - 3

ER -

Dicer is essential for mouse development

Abstract

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