A spontaneous autosomal recessive mutation causing disordered morphogenesis of the adrenal cortex has been identified in DW/J inbred strain mice and named adrenocortical dysplasia (acd). The acd mutant gene has been mapped just proximal to oligosyndactyly (Os) and esterase-1 (Es-1) in the central region of chromosome 8. Both male and female acd/acd mice are characterized by reduced survival, retarded growth, skin hyperpigmentation, poorly developed pelage and focal ureteral blockage leading to hydronephrosis. Morphometric measurements showed that acd/acd cortical cells and nuclei were increased sevenfold in volume; nuclei often showed a variety of inclusions. Cortical cells of acd/acd mice contained large numbers of mitochondria, smooth endoplasmic reticulum and lipid droplets characteristic of steroidogenic cells. While cortical X-zones failed to develop in acd/acd adrenals, medullary cells and nuclei were unaffected by mutant gene action. Resting serum corticosterone levels in female, but not male, mutant mice were significantly lower than in +/? normal littermates, whereas ACTH levels were significantly elevated in mutants of both sexes. Serum aldosterone levels were normal in acd/acd mice. Functional studies of adrenals cultured in vitro revealed that acd/acd adrenals secreted reduced amounts of corticosterone per pair of glands under both basal and ACTH-stimulated conditions. However, correction of the corticosterone secretion data to mg cortical mass in culture showed that the mutant cortical tissue secreted the same amount of glucocorticoid as did their +/? normal littermate glands. We conclude that the acd mutant gene acts in an unknown fashion to cause a fundamental defect in cellular proliferation in the adrenal cortex, leading to compensatory marked hypertrophy of cortical cells and grossly enlarged nuclei. The role of acd action in adrenal cortical development remains to be established.

Eggs from

Marked differences were found in the absolute and relative weights of the testes of young adult mice from 11 strains. DBA/2J mice had large testes (936 \m=+-\46 mg/100 g body weight) and C57BL/10J mice had small ones (389 \m=+-\6 mg/100 g). Comparisons of mice from these two strains, raised under three different environmental conditions, showed that the difference between the strains was relatively unaffected by environmental variation. Measurements on hybrid mice confirmed that much of the observed difference between the two strains was genetic in origin.The C57BL/10 mice were unlike those of any of the other strains in that both the relative and the absolute weights of the testis declined between the ages of 9 and 16 weeks.Strain differences were also found when spermatogenesis was studied in four of the strains by counting the different types of germinal cells in seminiferous tubules in stage VII of spermatogenesis. There were about twice as many type A spermatogonia in DBA/2 mice as there were in C57BL/10 mice. The mean numbers of spermatocytes and spermatids were much greater in DBA/2 than in C57BL/10. These differences were sufficient to account for the observed differences between these strains in testicular weight.Reciprocal F1 mice resembled their DBA/2 parents both in the weight of their testes and in the pattern of spermatogenesis.

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A spontaneous autosomal mutation in C57BL/Tb mice, provisionally called reduced pigmentation, symbol rp, has pronounced effects on three kidney lysosomal glycosidase activities. Homozygous rprp mice have significantly higher activities of /?-galactosidase, /?-glucuronidase and ly-acetyl-ZMiexosaminidase than their heterozygous litter-mates. Horaozygotes have light ears and tails, diluted fur and dark eyes. The mutation is not allelic to any known to affect lysosomal functions, or to a number of pigmentation variants with similar phenotypic effects. The locus is on chromosome 7.