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Gene-teratogen interaction in insulin-induced mouse exencephaly

W A Cole, D G Trasler

    Teratology
    |August 1, 1980
    PubMed
    Summary
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    Genomics·1993

    Mutant genes increase embryo sensitivity to insulin, leading to a higher incidence of exencephaly (a birth defect). This gene-teratogen interaction affects neural tube closure and embryonic development.

    Area of Science:

    • Developmental biology
    • Genetics
    • Teratology

    Background:

    • Mutant genes crooked (Cd) and rib fusion (Rf) in mice cause minor skeletal defects.
    • Teratogens, such as insulin, can induce birth defects.

    Purpose of the Study:

    • To investigate the interaction between heterozygous mutant genes and insulin teratogenicity.
    • To determine if mutant heterozygotes exhibit increased sensitivity to insulin-induced exencephaly.

    Main Methods:

    • Crossed mutant mouse strains (Cd or Rf) with A/J or SWV strains.
    • Treated pregnant mothers with teratogenic doses of insulin.
    • Analyzed F1 offspring for skeletal defects and exencephaly.
    • Performed dose-response curves and probit regression analysis.

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  • Examined embryonic turning, neural tube closure, and cell proliferation histologically.

    • Main Results:

    • Mutant heterozygotes exposed to insulin showed significantly higher rates of exencephaly compared to nonmutants.
    • Gene-teratogen interaction was confirmed by nonparallel probit regression lines.
    • Insulin delayed embryonic turning and neural tube closure, particularly in exencephalic embryos.
    • Reduced neurectoderm cell proliferation and mitotic index were observed in exencephalic embryos.

    Conclusions:

    • Heterozygous mutant genes confer increased sensitivity to insulin-induced exencephaly.
    • Delayed embryonic turning may be a mechanical factor in the failure of neural tube closure.
    • Insulin impacts neurectoderm development, leading to exencephaly in susceptible embryos.