The recently discovered lethal cab mutation in the mouse causes severe glycogen deficiency in affected homozygotes in addition to structural and functional abnormalities in the heart, lung, and liver. We propose to study the biochemical basis of this defect in carbohydrate metabolism by measuring the activity of key enzymes involved in glycogen synthesis and degradation in mutant fetuses. A physiological analysis will include studies of hormone sensitivity in normal adult heterozygotes and in cultured cells from the homozygous mutant fetus. A detailed ultrastructural examination of cab/cab, plus cab and plus/plus organs is also planned, along with experiments designed to permit determination of when the abnormal phenotype is first expressed during development. These studies may provide information on the genetic control of fetal metabolism and the morphological consequences which may result from its derangement.