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Contrasted, a steel allele in the mouse with intermediate effects

Published online by Cambridge University Press:  14 April 2009

C. V. Beechey  and
A. G. Searle
C. V. Beechey
Affiliation:
Medical Research Council, Radiobiology Unit, Harwell, Didcot, Oxon OX11 0RD
A. G. Searle
Affiliation:
Medical Research Council, Radiobiology Unit, Harwell, Didcot, Oxon OX11 0RD
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The steel allele, contrasted (Slcon), arose in a neutron irradiation experiment. Slcon is fully penetrant and heterozygotes can be recognized at or soon after birth by darkly pigmented external genitalia in both sexes, while the adult coat tends to be a little lighter than normal. Homozygotes also have dark genitalia and a markedly diluted coat. Both eumelanin and phaeomelanin are affected, with reduced numbers of cortical and medullary pigment granules in the hairs. Contrasted also affects the haematopoietic system, causing slight macrocytic anaemia in the homozygote. Slcon homozygous males are fertile but testes weigh on average 20% less than in their heterozygous litter-mates. Homozygous females are usually sterile although if mated early (4½−6 weeks) they occasionally have a single litter. Ovarian sections showed a gradual degeneration of oocytes in Graafian follicles so that most had gone by 2 months. Similarly, vaginal smears indicated that after about three normal cycles homozygous females lapsed into a state of persistent dioestrus; injections with gonadotrophins did not prolong their period of fertility or cause a resumption of their oestrous cycles. The effects on fertility, pigmentation and haematology of contrasted when combined with other steel alleles are also described.

Type
Research Article
Information
Genetics Research , Volume 42 , Issue 2 , October 1983 , pp. 183 - 191
Copyright
Copyright © Cambridge University Press 1983

References

REFERENCES

Batchelor, A. L., Phillips, R. J. S. & Searle, A. G. (1966). A comparison of the mutagenic effectiveness of chronic neutron- and Υ-irradiation of mouse spermatogonia. Mutation Research 3, 218–229.Google Scholar
Bennett, D. (1956). Developmental analysis of a mutation with pleiotropic effects in the mouse. Journal of Morphology 98, 199–229.CrossRefGoogle Scholar
Bloom, J. L. & Falconer, D. S. (1966). “Grizzled”, a mutant in linkage group X of the mouse. Genetical Research 7, 159–167.Google Scholar
Geschwind, I. I., Huseby, R. A. & Nishioka, R. (1972). The effect of melanocyte-stimulating hormone on coat colour in the mouse. Recent Progress in Hormone Research 28, 91–130.Google ScholarPubMed
Green, M. C. (1981). Genetic Variants and Strains of the Laboratory Mouse. Stuttgart: Gustav Fischer Verlag.Google Scholar
Grüneberg, H. (1969). Threshold phenomena versus cell heredity in the manifestation of sex linked genes in mammals. Journal of Embryology and Experimental Morphology 22, 145–179.Google ScholarPubMed
Mayer, T. C. (1973). Site of gene action in steel mice: analysis of the pigment defect by mesoderm-ectoderm recombinations. Journal of Experimental Zoology 184, 345–352.Google Scholar
Mayer, T. C. & Green, M. C. (1968). An experimental analysis of the pigment defect caused by mutations at the W and Sl loci in mice. Developmental Biology 18, 62–75.Google Scholar
McCoshen, J. A. & McCallion, D. J. (1975). A study of primordial germ cells during their migratory phase in steel mutant mice. Experientia 31, 589–590.Google Scholar
McCulloch, E. A., Siminovitch, J. E., Till, J. E., Russell, E. S. & Bernstein, S. E. (1965). The cellular basis of the genetically determined hemopoietic defect in anemic mice of genotype Sl/Sl d. Blood 26, 399–410.CrossRefGoogle ScholarPubMed
Mintz, B. (1970). Gene expression in allophenic mice. In Control Mechanisms in the Expression of Cellular Phenotypes (ed. Podylkula, H.), pp. 15–42. New York: Academic Press.Google Scholar
Riley, P. A. (1974). Pathological disturbances of pigmentation. In The Physiology and Pathophysiology of the Skin, vol. 3 (ed. Jarrett, A.), pp. 1167–1197. London: Academic Press.Google Scholar
Roderick, T. H. & Davisson, M. T. (1981). Linkage map, in Genetic Variants and Strains of the Laboratory Mouse (ed. Green, M. C.), pp. 279–282.Stuttgart: Gustav Fischer Verlag.Google Scholar
Russell, E. S. (1979). Hereditary anaemias of the mouse: a review for geneticists. Advances in Genetics 20, 397–459.Google Scholar
Searle, A. G. & Beechey, C. V. (1974). Sperm count, egg fertilization and dominant lethality after X-irradiation of mice. Mutation Research 22, 63–72.CrossRefGoogle ScholarPubMed
Searle, A. G. & Beechey, C. V. (1978). Complementation studies with mouse translocations. Cytogenetics and Cell Genetics 20, 282–303.Google Scholar
Silvers, W. K. (1979). The Coat Colours of Mice: a Model for Mammalian Gene Action and Interaction. New York: Springer Verlag.Google Scholar
Snell, R. S. & Bischitz, P. Z. (1963). Melanocytes and melanin in human abdominal wall skin: a survey made at different ages in both sexes and during pregnancy. Journal of Anatomy 97, 361–376.Google Scholar
Wallis, M. (1975). The molecular evolution of pituitary hoemones. Biological Reviews 50, 35–98.CrossRefGoogle Scholar