Abstract
Further studies of the four radiation-induced lethal albino mutations causing glucose 6-phosphatase deficiency in the mouse have shown that there is also a deficiency of tyrosine aminotransferase in the newborn albino mutants. These two enzymes can be induced in fetal and newborn heterozygous or homozygous normal littermate controls by injection of glucagon or dibutyryl cyclic AMP, but not in the albino mutants. Microsomal NADH-cytochrome c reductase was found to be increased in the albino mutants. The multiple biochemical abnormalities in the albino mutants, in addition to the lack of gene dosage effect in the heterozygotes, suggest the involvement of genes other than the structural genes for particular enzymes. When a new radiation-induced lethal albino mutation was tested against the four original alleles, complementation resulted, and double heterozygotes were found to be viable, with normal enzyme levels.
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