Mice lacking Dad1, the defender against apoptotic death-1, express abnormal N-linked glycoproteins and undergo increased embryonic apoptosis
Mice lacking Dad1, the defender against apoptotic death-1, express abnormal N-linked glycoproteins and undergo increased embryonic apoptosis
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DOI：
10.1006/dbio.2000.9615
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发表时间：
2000-04-01
影响因子：
2.7
通讯作者：
Winoto, A
中科院分区：
文献类型：
--
作者：
Hong, NA;Flannery, M;Winoto, A
Dad 1已被证明在防止凋亡性细胞死亡和调节酿酒酵母和BHK仓鼠细胞系中的N-连接糖基化水平中起作用。为了解决Dad 1在多细胞发育过程中在这些过程中的体内作用，我们分析了携带Dad 1无效等位基因的小鼠。这种突变的纯合子胚胎表达异常的N-糖基化蛋白，并在胚胎7.5天发育延迟。这种突变体表现出异常的形态，受损的中胚层发育，并在特定组织中增加细胞凋亡的水平。这些缺陷最终导致纯合子胚胎不能转动后轴，随后在胚胎第10.5天死亡。因此，Dad 1是必需的N-连接的糖蛋白的适当加工和某些细胞存活的小鼠。(C)北京大学出版社.
Dad1 has been shown to play a role in preventing apoptotic cell death and in regulating levels of N-linked glycosylation in Saccharomyces cerevisiae and the BHK hamster cell line. To address the in vivo role of Dad1 in these processes during multicellular development, we have analyzed mice carrying a null allele for Dad1. Embryos homozygous for this mutation express abnormal N-glycosylated proteins and are developmentally delayed by embryonic day 7.5. Such mutants exhibit aberrant morphology, impaired mesodermal development, and increased levels of apoptosis in specific tissues. These defects culminate in homozygous embryos failing to turn the posterior axis and subsequent lethality by embryonic day 10.5. Thus, Dad1 is required for proper processing of N-linked glycoproteins and for certain cell survival in the mouse. (C) 2000 Academic Press.