Analysis of the syndrome of congenital malformations induced in genetically defined mice by acute riboflavin deficiency.
The role of genetics in the expression of a complex syndrome of teratologically induced congenital malformations was examined by the use of three inbred strains and 15 related crosses of mice. The syndrome, which included various limb, brain, orofacial, gastrointestinal, and miscellaneous malformations, was induced by an intense riboflavin deficiency produced by feeding the antagonist galactoflavin during midgestation. Analyses of the data showed that, although all three strains shared the major and most other features of the syndrome, there occurred in its manifestation vast quantitative and qualitative differences among them, in which they were resembled by their related crosses such as to constitute strain-specific malformation patterns. The results can be regarded as typifying an animal counterpart of human situations, the three strains representing in toto the mouse family, each strain individually exhibiting the variety that occurs between siblings in expressing a single syndrome.
Kalter
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Children's Hospital Medical Center, Cincinnati, OH 45229.
D000208:Acute Disease; D000818:Animals; D003433:Crosses, Genetic; D004435:Eating; D005145:Face / Q000002:abnormalities; D017880:Limb Deformities, Congenital; D008098:Litter Size; D051379:Mice; D008815:Mice, Inbred Strains; D012256:Riboflavin / Q000031:analogs & derivatives / Q000037:antagonists & inhibitors / Q000633:toxicity; D012257:Riboflavin Deficiency / Q000139:chemically induced / Q000151:congenital* / Q000235:genetics; D013723:Teratogens
D013723:Teratogens; D012256:Riboflavin; C007811:galactoflavin