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Related Experiment Videos

Interactions between cycloheximide and T-locus alleles during mouse embryogenesis

J M Lary, R D Hood, R Lindahl

    Teratology
    |June 1, 1982
    PubMed
    Summary

    Cycloheximide exposure during pregnancy caused birth defects in mice, particularly in those with genetic mutations like brachyury (T). These mutations enhanced the drug's teratogenic effects, increasing malformations and prenatal mortality.

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    Area of Science:

    • Developmental Biology
    • Toxicology
    • Genetics

    Background:

    • The brachyury (T) gene is crucial for embryonic development, affecting tail length and potentially other developmental processes.
    • Genetic background can influence the expressivity of genes, as observed with the T gene in CD-1 mice.
    • Cycloheximide is a known teratogen, but its effects can be modulated by genetic factors.

    Purpose of the Study:

    • To investigate the teratogenic effects of cycloheximide in mice with different genetic backgrounds, specifically focusing on the brachyury (T) gene and its alleles.
    • To determine if the T gene or its alleles (T/+ or tw18/+) enhance the teratogenicity of cycloheximide.
    • To assess the impact of cycloheximide on fetal development, including malformations, prenatal mortality, and tail length.

    Main Methods:

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    • Mating of female CD-1 mice with F1 males carrying either the T/+ or tw18/+ alleles, or wild-type (+/+) alleles.
    • Injection of pregnant mice on gestation Day 9 with cycloheximide (30 mg/kg) or left untreated.
    • Examination of fetuses on gestation Day 17 for gross malformations, skeletal abnormalities, taillessness, and body weight.

    Main Results:

    • Cycloheximide induced teratogenic effects across all genetic crosses, including polydactyly, oligodactyly, and skeletal abnormalities.
    • Mutant-containing litters (T/+ and tw18/+) showed increased gross and skeletal malformations compared to wild-type (+/+) litters after cycloheximide exposure.
    • Prenatal mortality and decreased fetal weights were observed in treated mutant litters, and taillessness increased in T/+ litters.

    Conclusions:

    • Both T and tw18 alleles appear to enhance the teratogenicity of cycloheximide in mice.
    • Cycloheximide may increase the expressivity of the T gene, leading to more severe developmental defects.
    • Genetic factors play a significant role in modulating the response to teratogenic agents during embryonic development.