Growth hormone and prolactin synthesis in normal and homozygous Snell and Ames dwarf mice.
The severe growth retardation and sterility characteristic of Snell and Ames dwarfs, two nonallelic, recessive mouse mutants, have been attributed to a deficiency in pituitary production of GH and PRL. We have investigated the synthesis of these hormones in normal and homozygous dwarf mice of both strains at various stage of development to determine whether the mutations prevent initial development of the pituitary capacity to produce these hormones. Synthesis of radiolabeled GH and PRL was assayed by two-dimensional electrophoresis and immunoprecipitation using goat antisera to mouse GH and PRL. Litters in which all pups were mutant were produced by mating adult dwarfs made fertile by implanting a normal pituitary under the kidney capsule. We found that GH and PRL synthesis was undetectable in Snell or Ames dwarfs at all stages of development examined, including the neonatal period when dwarf pups are indistinguishable from normal littermates. Furthermore, we detected no immunoprecipitable peptides which might represent mutant hormones in these animals. Assays of GH synthetic rates in heterozygous animals indicated that there may be a slight negative effect of the mutant gene on GH synthesis in Snell animals. It was concluded that in the homozygous condition, both types of dwarf alleles result in failure of the pituitary to initiate GH and PRL synthesis.
D000483:Alleles; D000818:Animals; D004392:Dwarfism / Q000235:genetics / Q000378:metabolism*; D005838:Genotype; D013006:Growth Hormone / Q000096:biosynthesis*; D006720:Homozygote; D051379:Mice; D008817:Mice, Mutant Strains; D010902:Pituitary Gland / Q000378:metabolism*; D011388:Prolactin / Q000096:biosynthesis*
D011388:Prolactin; D013006:Growth Hormone