| First Author | Nishii K | Year | 1999 |
| Journal | Genes Cells | Volume | 4 |
| Issue | 4 | Pages | 243-52 |
| PubMed ID | 10336695 | Mgi Jnum | J:99897 |
| Mgi Id | MGI:3584199 | Doi | 10.1046/j.1365-2443.1999.00256.x |
| Citation | Nishii K, et al. (1999) Abnormalities of developmental cell death in Dad1-deficient mice. Genes Cells 4(4):243-52 |
| abstractText | 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. RESULTS: To determine the role of Dad1 function in vivo, we prepared by gene targeting, mice harbouring a disrupted Dad1 gene. Homozygous mutants died shortly after they were implanted with the characteristic features of apoptosis. In an in vitro blastocyst culture system, Dad1-null cells displayed abnormalities which were comparable to those obtained in vivo. However, oligosaccharyltransferase activity was apparently retained even after the Dad1-null cells were destined to die. Some live-born heterozygous mutants displayed soft-tissue syndactyly. Mild thymic hypoplasia was also indicated in heterozygotes. CONCLUSION: These results suggest the involvement of the Dad1 gene in the acquisition of a common syndactyly phenotype, as well as in the control of programmed cell death during development. |
