Genetically determined organ specific responses to the teratogenic action of 6-aminonicotinamide in the mouse

Abstract

1. A two-hour relative deficiency of nicotinamide, produced by maternal treatment with 6-aminonicotinamide, resulted in a maximum frequency of vertebral fusions following treatment on day 9·5 of gestation, and a maximum frequency of cleft palates following treatment on day 13·5.2. Both defects appeared with higher frequencies in the A/Jax than in the C57BL/6J inbred strain.3. The frequency of induced vertebral fusions in F1embryos from crosses between the strains was higher when the father was from the A/Jax strain than when the mother was—a patroclinous reciprocal cross difference.4. The frequency of induced cleft palate in F1embryos from crosses between the strains was higher when the mother was from the A/Jax strain than when the father was—a matroclinous reciprocal cross difference.5. Since the reciprocal cross differences in frequency of vertebral fusions and for cleft palates were in opposite directions, the hereditary factors influencing susceptibility to the teratogen appear to differ for the respective organ anlage. These differences appear to be, in part, cytoplasmic.6. The frequency of induced cleft palate in the offspring of backcrosses of (untreated) F1female hybrids to A/Jax males differed according to the cytoplasmic origin of the F1mothers. Thus the susceptibility of an embryo to the teratogen appears to be influenced by factors transmitted through the cytoplasm.