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• W2003185547 abstract "Background: Many birth defects are believed to involve gene–environment interactions, although the mechanisms involved are poorly understood. Apoptosis is a common effect of many kinds of environmental stresses on the developing embryo; therefore, mechanisms of teratogenesis may be approached within the context of the cell death program. The p53 tumor suppressor gene encodes a transcription factor which functions as a critical regulator of apoptosis in response to environmental stress.Results To investigate the relationship between p53-dependent apoptosis and teratogenesis, we subjected day 8 mouse embryos with different p53 gene backgrounds to a genotoxic stress, 2-chloro-2′-deoxyadenosine. Treatment rapidly stimulated nuclear p53 accumulation and triggered apoptosis in some (head-fold) but not other (primitive heart) developing structures. Induced cell death was p53 gene-dose dependent, as shown by the intermediate sensitivity of 4–5 somite stage embryos bearing only a single effective p53 allele and the lack of sensitivity of p53-null mutants. Abnormal development was manifested as eye defects by day 11, particularly lens agenesis. Overall the incidences of these defects at term were 73.3 % for p53 wild-type fetuses, 52.5 % for heterozygous mutants, and 2.2 % for p53-null mutants. Statistical analysis indicated that the interaction between teratogen and genotype was highly significant (P ≤ 0.001) for cell death on day 8 and eye defects on day 17.Conclusion We conclude that teratogen induction of p53-dependent apoptosis in the developing embryo is positively coupled to the determination of congenital eye defects." @default.
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• W2003185547 date "1996-01-01" @default.
• W2003185547 modified "2023-09-30" @default.
• W2003185547 title "Teratogen-induced eye defects mediated by p53-dependent apoptosis" @default.
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• W2003185547 doi "https://doi.org/10.1016/s0960-9822(02)00422-0" @default.
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