Dicer is essential for mouse development.
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.
Bernstein
Emily
E
Cold Spring Harbor Laboratory, Watson School of Biological Sciences, 1 Bungtown Road, Cold Spring Harbor, New York 11724, USA.
Kim
Sang Yong
SY
Carmell
Michelle A
MA
Murchison
Elizabeth P
EP
Alcorn
Heather
H
Li
Mamie Z
MZ
Mills
Alea A
AA
Elledge
Stephen J
SJ
Anderson
Kathryn V
KV
Hannon
Gregory J
GJ
D000595:Amino Acid Sequence; D000818:Animals; D053487:DEAD-box RNA Helicases; D005314:Embryonic and Fetal Development / Q000502:physiology*; D004722:Endoribonucleases / Q000235:genetics / Q000502:physiology*; D051379:Mice; D018345:Mice, Knockout; D008969:Molecular Sequence Data; D020365:RNA Helicases / Q000235:genetics / Q000502:physiology*; D034622:RNA Interference; D043244:Ribonuclease III; D013234:Stem Cells / Q000166:cytology
D004722:Endoribonucleases; C408087:DICER1 protein, human; D043244:Ribonuclease III; D053487:DEAD-box RNA Helicases; D020365:RNA Helicases