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6-Aminonicotinamide-induced cleft palate in the mouse: the nature of the difference between the A/J and C57Bl/6J

F G Biddle

    Teratology
    |December 1, 1977
    PubMed
    Summary

    Genetic differences in mouse strains affect cleft palate susceptibility to 6-aminonicotinamide (6-AN). Mouse strains exhibit varying dosage tolerance to 6-AN, influencing cleft palate induction.

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    Area of Science:

    • Developmental biology
    • Genetics
    • Toxicology

    Background:

    • Cleft palate is a common birth defect.
    • Environmental factors and genetic predisposition contribute to its development.
    • 6-aminonicotinamide (6-AN) is a known teratogen that can induce cleft palate in animal models.

    Purpose of the Study:

    • To investigate the genetic basis for differences in cleft palate induction by 6-AN between A/J and C57BL/6J mouse strains.
    • To determine the nature of strain differences in response to 6-AN exposure.

    Main Methods:

    • Administered varying doses of 6-AN to pregnant A/J and C57BL/6J mice.
    • Utilized probit analysis to quantify cleft palate response and determine dose-response curves.
    • Examined genetic additivity and dominance deviations in F1 embryos.

    Main Results:

    • Identified parallel dose-response curves for cleft palate induction, indicating differences in dosage tolerance (log ED50) between strains.
    • Found no evidence of maternal cytoplasmic effects influencing 6-AN-induced cleft palate.
    • Observed a departure from genetic additivity and suggested dominance deviation in F1 embryos towards the C57BL/6J strain.

    Conclusions:

    • A3-locus epistatic model proposed to explain strain differences in embryonic tolerance to 6-AN.
    • Genetic factors, potentially linked to the brown (b) locus, underlie differential susceptibility to 6-AN-induced cleft palate.