Deletion of Dad1 in mice induces an apoptosis-associated embryonic death

被引:5
|
作者
Brewster, JL
Martin, SL
Toms, J
Goss, D
Wang, K
Zachrone, K
Davis, A
Carlson, G
Hood, L
Coffin, DJ
机构
[1] Pepperdine Univ, Div Nat Sci, Malibu, CA 90263 USA
[2] Stowers Inst Med Res, Kansas City, MO USA
[3] McLaughlin Res Inst Biomed Sci, Great Falls, MT USA
[4] Darwin Mol Grp, Bothell, WA USA
[5] Univ Washington, Dept Mol Biotechnol, Seattle, WA 98195 USA
[6] Univ Montana, Dept Pharmaceut Sci, Missoula, MT 59812 USA
关键词
Dad1; embryonic apoptosis; gene targeting; T-cell receptor;
D O I
10.1002/(SICI)1526-968X(200004)26:4<271::AID-GENE90>3.3.CO;2-5
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Dad1is a putative anti-apoptosis gene identified in several distantly related organisms. Expression of Dad1 in transfected cells inhibits apoptosis in vitro. To determine whether Dad1 has a similar function in vivo, we used gene targeting to delete Dad1. Heterozygous adult mice (+/-) show no obvious phenotype or abnormalities, but genotype analysis of over 100 offspring from heterozygous matings detected no weanling, homozygous Dad1 null (-/-) mice. Subsequent analysis of embryos from heterozygous matings detected Dad1 null (-/-) embryos at E3.5 but no later, suggesting Dad1 is required for development beyond the late blastocyst stage. Increased levels of apoptosis were observed in cultured embryos lacking a functional copy of the gene, consistent with an anti-apoptotic role for Dad1. genesis 26:271-278, 2000. (C) 2000 Wiley-Liss, Inc.
引用
收藏
页码:271 / 278
页数:8
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