Abnormalities of developmental cell death in Dad1‐deficient mice

Abstract

Background: Dad1, the defender against apoptotic cell death, comprises the oligosaccharyltransferase complex and is well conserved among eukaryotes. In hamster BHK21-derived tsBN7 cells, loss of Dad1 causes apoptosis which cannot be prevented by Bcl-2.

Cell death in the absence of Bax and Bak

“…9 However, the individual contribution of these genes can be hard to evaluate either because the interdigital tissue is ultimately resorbed or the embryos die before birth. 10,11 In contrast, as shown in Figure 1a, the bax À/À bak À/À mice display the persistence of interdigital webs into adulthood. 7 This phenotype is observed in all bax À/À bak À/À mice.…”

Ultraviolet-C Overexposure Induces Programmed Cell Death in Arabidopsis, Which Is Mediated by Caspase-like Activities and Which Can Be Suppressed by Caspase Inhibitors, p35 and Defender against Apoptotic Death

“…In contrast, this protein was suggested to have a suppressor activity in PCD by studies in Caenorhabditis elegans, where its overexpression protects some of the cells destined to die by apoptosis during development (47). In addition, knockout mutants in mice show an increased level of apoptosis in cultured embryos (48) or an altered interdigital cell death in heterozygotes (49), suggesting a role for DAD1 in developmental PCD. All these results favor a direct or indirect anti-apoptotic role for this gene in animal apoptosis.…”

Effects of environmental enrichment on gene expression in the brain

“…DAD1 is a subunit of the oligosaccharyltransferase complex that initiates N-linked glycosylation. Mice harboring a disrupted dad1 gene exhibit abnormal cell death, and the homozygous deleted mice die soon after implantation (50), implicating DAD1 in the control of programmed cell death during development. Changes in the expression of DAD1, like caspase 6 and Bax, during enrichment may play an important antiapoptotic role.…”