Experimental teratological studies with the mouse CNS mutations cranioschisis and delayed splotch.
Teratological experiments were made with a recessive mouse gene (cranioschisis) causing exencephaly and a semidominant gene (delayed splotch) causing spina bifida. In studies with the cranioschisis gene administration of warfarin and thyroxine resulted in frequencies of exencephaly significantly below that expected of a recessive trait, perhaps indicating selective elimination of abnormal conceptuses. Studies with the delayed splotch gene tested the hypothesis that offspring with a hereditary defect of neural-tube closure have other, unexpressed CNS defects, which may be elicited by teratological impulses. This proposition was decisively upheld by administering 5-bromo-2'-deoxyuridine, cadmium sulfate and retinoic acid, as these treatments all caused significantly greater frequencies of induced exencephaly in offspring with spina bifida than in their genetically normal littermates.
D000818:Animals; D001973:Bromodeoxyuridine / Q000633:toxicity; D002104:Cadmium / Q000633:toxicity; D019187:Cadmium Compounds; D005260:Female; D005799:Genes, Dominant / Q000187:drug effects*; D005808:Genes, Recessive / Q000187:drug effects*; D051379:Mice; D009154:Mutation; D011247:Pregnancy; D012886:Skull / Q000002:abnormalities* / Q000187:drug effects; D016136:Spina Bifida Occulta / Q000139:chemically induced / Q000235:genetics*; D013431:Sulfates; D013723:Teratogens / Q000633:toxicity*; D013974:Thyroxine / Q000633:toxicity; D014212:Tretinoin / Q000633:toxicity; D014859:Warfarin / Q000633:toxicity
D019187:Cadmium Compounds; D013431:Sulfates; D013723:Teratogens; D002104:Cadmium; D014212:Tretinoin; D014859:Warfarin; C037123:cadmium sulfate; D001973:Bromodeoxyuridine; D013974:Thyroxine