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High frequency of a lethal gene (te) in a laboratory stock of mice

Published online by Cambridge University Press:  14 April 2009

Nigel Bateman
Nigel Bateman
Affiliation:
Agricultural Research Council's Animal Breeding Research Organisation, Edinburgh 9
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A long-established laboratory stock was found to contain many individuals that were heterozygous for a lethal gene, called tailless-Edinburgh (te). Heterozygotes are indistinguishable from normals except by breeding tests with special tester stocks supplying brachyury (T) gametes, when tailless (Tte) progeny distinguish carrier parents from normal parents that produce only short-tailed (T +) progeny. When males are mated to tester females providing brachyury eggs, the ratio of Tte: T + progeny reflects the ratio of te: + spermatozoa. The proportion of te spermatozoa measured in this way led to the expectation that 62% of individuals in the original stock would be carriers, whereas 80% was found. Independent evidence is presented for + te males that the incidence of te in their effective spermatozoa was higher when normal eggs were fertilized in matings within the original stock than when brachyury eggs were fertilized in outcross matings to the tester stock. These observations suggest that the proportion of te spermatozoa partaking in fertilization was modified by the genotypes of the females or of their eggs.

Type
Research Article
Information
Genetics Research , Volume 1 , Issue 2 , July 1960 , pp. 214 - 225
Copyright
Copyright © Cambridge University Press 1960

References

REFERENCES

Bateman, N. (1957). Research notes. Two new mutants. Mouse News Letter., 16, 7. (Produced for limited circulation by Intern. Cttee on Lab. Animals, M.R.C. Laboratories, Carshalton, Surrey.)Google Scholar
Bruck, D. (1957). Male segregation ratio advantage as a factor in maintaining lethal alleles in wild populations of house mice. Proc. Nat. Acad. Sci., Wash., 43, 152–158.CrossRefGoogle ScholarPubMed
Dunn, L. C. (1957). Evidence of evolutionary forces leading to the spread of lethal genes in wild populations of house mice. Proc. Nat. Acad. Sci., Wash., 43, 158–163.CrossRefGoogle Scholar
Dunn, L. C., Beasley, A. B. & Tinker, H. (1958). Relative fitness of wild house mice heterozygous for a lethal gene. Amer. Nat. 92, 215–220.CrossRefGoogle Scholar
Dunn, L. C. & Glueckshon-Schoenheimer, S. (1950). Repeated mutations in one area of a mouse chromosome. Proc. Nat. Acad. Sci., Wash., 36, 233–237.CrossRefGoogle ScholarPubMed
Prout, T. (1953). Some effects of variations in the segregation ratio and of selection on the frequency of alleles under random mating. Acta Genet. 4, 148–151.Google ScholarPubMed
Lyon, M. F. (1959). A new dominant T-allele in the house mouse. J. Hered. 50, 140–142.CrossRefGoogle Scholar
Lyon, M. F. (1960). Personal communication. Mouse News Letter, 22, 30.Google Scholar