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Genetics of clefting in the mouse
Progress in Clinical and Biological Research
|January 1, 1980
Summary
The study investigated if A/J mice share a common mechanism for teratogen sensitivity. Findings suggest independent genetic systems for cyclophosphamide (CP) and 6-aminonicotinamide (6-AN) teratogenesis in A/J mice.
Area of Science:
- Developmental toxicology
- Immunogenetics
- Teratology
Background:
- The A/J mouse strain exhibits heightened sensitivity to various teratogens.
- Previous research suggested independent mechanisms for teratogen induction by cortisone and 6-aminonicotinamide (6-AN).
Purpose of the Study:
- To explore whether the sensitivity of A/J mice to cyclophosphamide (CP) and other teratogens is mediated by a common underlying mechanism.
- To further elucidate the genetic basis of teratogen response differences between mouse strains.
Main Methods:
- Comparative analysis of teratogen response in A/J mice.
- Genetic modeling to explain strain differences in teratogen sensitivity.
- Association studies with the H-2 complex.
Main Results:
- The genetic basis for 6-AN teratogenesis in A/J mice was proposed to involve three embryonic loci with dominance and epistasis.
- Cortisone teratogenesis sensitivity in A/J mice was attributed to two loci with independent effects and a maternal effect.
- A portion of the maternal effect and one embryonic locus for cortisone response were linked to the H-2 complex.
Conclusions:
- The teratogenic effects of cyclophosphamide and 6-aminonicotinamide in A/J mice likely arise from distinct genetic mechanisms.
- Genetic factors, including maternal effects and loci associated with the H-2 complex, contribute to differential teratogen sensitivity.