Hostname: page-component-586b7cd67f-2plfb Total loading time: 0 Render date: 2024-11-28T07:01:59.086Z Has data issue: false hasContentIssue false

Diabetes insipidus associated with oligosyndactyly in the mouse

Published online by Cambridge University Press:  14 April 2009

D. S. Falconer
Affiliation:
A.R.C. Unit of Animal Genetics, Institute of Animal Genetics, Edinburgh
M. Latsyzewski
Affiliation:
A.R.C. Unit of Animal Genetics, Institute of Animal Genetics, Edinburgh
J. H. Isaacson
Affiliation:
A.R.C. Unit of Animal Genetics, Institute of Animal Genetics, Edinburgh
Rights & Permissions [Opens in a new window]

Extract

Core share and HTML view are not available for this content. However, as you have access to this content, a full PDF is available via the ‘Save PDF’ action button.

1. A mild diabetes insipidus is associated with the oligosyndactyly caused by the dominant gene Os. No recombinants were observed between the diabetes and the oligosyndactyly so the diabetes is probably a pleiotropic effect of the Os gene.

2. There are one or more modifying genes which in combination with Os enhance the manifestation and cause a severe diabetes insipidus. This affects both sexes and becomes progressively worse in older animals, the average water intake reaching 50–60 ml. per 24 hours, or 1·7 times the body weight.

3. The modifying gene or genes, in the absence of the Os gene, themselves produce a mild diabetes insipidus, which becomes severe in some old females.

4. The severe diabetes insipidus associated with Os and the modifying genes together is probably renal in origin.

Type
Research Article
Copyright
Copyright © Cambridge University Press 1964

References

REFERENCES

Bartlett, M. S. & Haldaue, J. B. S. (1935). The theory of inbreeding with forced hetero-zygosis. J. Genet. 31, 327340.CrossRefGoogle Scholar
Forssman, H. (1955). Two different mutations of the X-chromosome causing diabetes insipidus. Amer. J. hum. Genet. 7, 2126.Google ScholarPubMed
Grüneberg, H. (1956). Genetical studies on the skeleton of the mouse. XVIII. Three genes for syndactylism. J. Genet. 54, 113145.CrossRefGoogle Scholar
Grüneberg, H. (1961). Genetical studies on the skeleton of the mouse. XXVII. The development of oligosyndactylism. Genet. Res. 2, 3342.CrossRefGoogle Scholar
Kadam, K. M. (1962). Genetical studies on the skeleton of the mouse. XXXI. The muscularanatomy of syndactylism and oligosyndactylism. Genet. Res. 3, 139156.CrossRefGoogle Scholar
Martin, F. I. R. (1959). Familial diabetes insipidus. Quart. J. Med. 28, 573582.Google ScholarPubMed
Sawyer, W. H., Valtin, H. & Sokol, H. W. (1964). Neurohypophysial principles in rats with familial hypothalamic diabetes insipidus (Brattleboro strain). Endocrinology, 74, 153155.CrossRefGoogle ScholarPubMed
Silverstein, E., Sokoloff, L., Mickelsen, O. & Jay, G. E. (1961). Primary polydipsia and hydronephrosis in an inbred strain of mice. Amer. J. Pathol. 38, 143158.Google Scholar
Valtin, H., Schroeder, H. A., Benirschke, K. & Sokol, H. (1962). Familial hypothalamic diabetes insipidus in rats. Nature, Lond., 196, 11091110.CrossRefGoogle ScholarPubMed