Abstract
The mammalian Daxx gene has been identified in a diverse set of yeast interaction trap experiments. Although a facilitating role for Daxx in Fas-induced apoptosis has been suggested, Daxx's physiologic function remains unknown. To elucidate the in vivo role of Daxx, we have generated Daxx-deficient mice. Surprisingly, rather than a hyperproliferative disorder expected from the loss of a pro-apoptotic gene, mutation of Daxx results in extensive apoptosis and embryonic lethality. These findings argue against a role for Daxx in promoting Fas-induced cell death and suggest that Daxx either directly or indirectly suppresses apoptosis in the early embryo.
MeSH terms
-
Adaptor Proteins, Signal Transducing
-
Animals
-
Apoptosis*
-
Carrier Proteins / genetics
-
Carrier Proteins / metabolism*
-
Cell Nucleus / metabolism
-
Cells, Cultured
-
Chromosomes / genetics
-
Cloning, Molecular
-
Co-Repressor Proteins
-
DNA Methylation
-
Embryo, Mammalian / cytology*
-
Embryo, Mammalian / metabolism
-
Embryonic and Fetal Development*
-
Exons / genetics
-
Female
-
Gene Deletion*
-
Genes, Essential / genetics
-
Genes, Lethal / genetics
-
Genotype
-
Humans
-
Intracellular Signaling Peptides and Proteins*
-
Male
-
Mice
-
Mice, Knockout
-
Molecular Chaperones
-
Nuclear Proteins*
-
O(6)-Methylguanine-DNA Methyltransferase / metabolism
-
Protein Binding
-
RNA, Messenger / genetics
-
RNA, Messenger / metabolism
Substances
-
Adaptor Proteins, Signal Transducing
-
Carrier Proteins
-
Co-Repressor Proteins
-
DAXX protein, human
-
Daxx protein, mouse
-
Intracellular Signaling Peptides and Proteins
-
Molecular Chaperones
-
Nuclear Proteins
-
RNA, Messenger
-
O(6)-Methylguanine-DNA Methyltransferase