Biochemical effects of the gene g on the development of the axolotl Ambystoma mexicanum

Abstract

Summary The recessive lethal geneg affects the late embryonic development of the axolotl,Ambystoma mexicanum. Mutant embryos show abnormal gills, slow yolk metabolism, and excessive xanthophore and melanophore pigmentation; they die, usually within 1 week after hatching. The biochemical abnormalities of mutant embryos were studied to discover the basis of the mutant syndrome. Thein vitro activity of esterases ofgg embryos and the electrophoretic properties of their isolated esterases are normal. However, theirin vivo activity is reduced, probably as a result of the defective attachment to membranes of at least one of the esterases. Other membrane bound enzymes may be affected similarly. Mutant embryos usually show an abnormally highin vitro andin vivo activity of the pentose shunt, and an abnormal accumulation of pteridines, suggesting a dependence upon “soluble” enzymes for energy. The plasma membranes of axolotl embryos are of two density classes. Mutant embryos have a large proportion of low density membrane material and little high density membrane material. Normal embryos have little low density membrane material and a large proportion of high density material. Less protein is detachable by electrophoresis from plasma membranes ofgg embryos than from the plasma membranes of normal embryos. The results support the hypothesis that the product of the normal allele is a membrane component or some other protein necessary for the attachment of proteins to membranes.