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Evidence for a major gene for rapid postweaning growth in mice

Published online by Cambridge University Press:  14 April 2009

G. E. Bradford  and
T. R. Famula
G. E. Bradford
Affiliation:
Animal Science Department, University of California, Davis, CA 95616
T. R. Famula
Affiliation:
Animal Science Department, University of California, Davis, CA 95616
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Mice gaining 3 or more standard deviations above the mean were noted beginning in generation 25 in a line selected for high 21–42 day weight gain. The exceptional growth rate appears to be due to an autosomal recessive gene, based on the following: (1) the exceptional individuals appeared suddenly, in only one of 2 closely related sublines; (2) mating high growth individuals to unrelated, normal size strains produces relatively uniform F1's with mean gains below the mid-parent average; (3) F2's have a distribution markedly skewed towards high gain and a coefficient of variation approximately double that of F1's; (4) true breeding high growth strains can be established in one generation by intermating the largest F2's; (5) intermating normal F2's produces progenies with a distribution similar to the F1 except for a few large segregates; (6) high growth segregates have been obtained in F2's from each of 4 successive backcrosses to the C57BL/6 inbred line. The symbol hg (high growth) is proposed for the postulated gene, which appears to be completely recessive. Frequency of positively identified segregates in F2's and backcrosses is on average less than 25 and 50%, due probably to some overlap of Hg- and hghg distributions. Gain of hghg individuals from 21–42 days is 30–50% higher than of Hg- contemporaries; mature weight is also much higher, while 21-day weight of hghg individuals in segregating litters is slightly lower. Fertility of homozygotes ranges from normal to as much as 40% lower than for comparable Hg- mice; hghg mice are not obese. The gene may provide a useful model for study of regulation of mammalian growth.

Type
Research Article
Information
Genetics Research , Volume 44 , Issue 3 , December 1984 , pp. 293 - 308
Copyright
Copyright © Cambridge University Press 1984

References

REFERENCES

Barria, N. & Bradford, G. E. (1981 a). Long-term selection for rapid gain in mice. I. Genetic analysis at the limit of response. Journal of Animal Science 52, 729–738.CrossRefGoogle ScholarPubMed
Barria, N. & Bradford, G. E. (1981 b). II. Correlated changes in reproduction. Journal of Animal Science 52, 739–747.CrossRefGoogle ScholarPubMed
Bradford, G. E. (1971). Growth and reproduction in mice selected for rapid body weight gain. Genetics 69, 499–512.CrossRefGoogle ScholarPubMed
Calvert, C. C., Famula, T. R. & Bradford, G. E. (1984). Composition of growth in mice with a major gene for rapid postweaning gain. Journal of Animal Science 59, 361–365.CrossRefGoogle Scholar
Eisen, E. J. (1974). The laboratory mouse as a mammalian model for the genetics of growth. Proc. 1st World Congress of Genetics Applied to Livestock Production 1, 467–492.Google Scholar
Eklund, J. & Bradford, G. E. (1976). A note on short-term selection for birth weight in mice. Animal Production 22, 127–130.Google Scholar
Eklund, J. & Bradford, G. E. (1977). Longevity and lifetime body weight in mice selected for rapid growth. Nature, 265 (5589), 48–49.CrossRefGoogle ScholarPubMed
Green, M. C. (1981). Catalog of mutant genes and polymorphic loci. In Genetic Variants and Strains of the Laboratory Mouse (ed. Green, M. C.). Stuttgart: Fisher.Google Scholar
Hanset, R. (1982). Major genes in animal production, examples and perspectives: cattle and pigs. Proc. 2nd World Congress of Genetics Applied to Livestock Production VI, 439–453.Google Scholar
McCarthy, J. C. (1982). The laboratory mouse as a model for animal breeding: a review of selection for increased body weight and litter size. Proc. 2nd World Congress of Genetics Applied to Livestock Production V, 66–83.Google Scholar
Palmiter, R. D., Norstedt, G., Gelinas, R. E., Hammer, R. E. & Brinster, R. L. (1983). Metallothionen-Human GH fusion genes stimulate growth in mice. Science 222, 809–814.CrossRefGoogle Scholar
Roberts, R. C. (1966). The limits to artificial selection for body weight in the mouse. I. The limits obtained in earlier experiments. Genetical Research 8, 347–360.CrossRefGoogle ScholarPubMed
Roberts, R. C. & Smith, C. (1982). Genes with large effects. Theoretical aspects in livestock breeding. Proc. 2nd World Congress of Genetics Applied to Livestock Production VI, 420–438.Google Scholar
Smith, C. & Bampton, P. R. (1977). Inheritance of reaction to halothane anesthesia in pigs. Genetical Research 29, 287–292.CrossRefGoogle ScholarPubMed
Spearow, J. L., Neira, R. & Bradford, G. E. (1976). Litter size and gain: selection and crossing effects. Journal of Animal Science 43, 222 (Abstr.).Google Scholar
Webb, A. J., Carden, A. E., Smith, C. & Imlah, P. (1982). Porcine stress syndrome in pig breeding. Proc. 2nd World Congress of Genetics Applied to Livestock Production V, 588–608.Google Scholar