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Nishii, K. et al.

Nishii, Tsuzuki, Kumai, Takeda, Koga, Aizawa, Nishimoto, Shibata,

Abnormalities of developmental cell death in Dad1-deficient mice.

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.[1]

References

Abnormalities of developmental cell death in Dad1-deficient mice. Nishii, K., Tsuzuki, T., Kumai, M., Takeda, N., Koga, H., Aizawa, S., Nishimoto, T., Shibata, Y. Genes Cells (1999) [Pubmed]

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