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Non-random X-chromosome inactivation in the mouse: difference of reaction to imprinting

Published online by Cambridge University Press:  14 April 2009

D. S. Falconer ,
J. H. Isaacson  and
I. K. Gauld
D. S. Falconer
Affiliation:
Institute of Animal Genetics, Edinburgh, EH9 3JN
J. H. Isaacson
Affiliation:
Institute of Animal Genetics, Edinburgh, EH9 3JN
I. K. Gauld
Affiliation:
Institute of Animal Genetics, Edinburgh, EH9 3JN
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Selection for increased and for decreased expression of the sex-linked gene brindled (Mobr) in heterozygous females produced two lines with non-random X chromosome inactivation. In the High line the X chromosome marked by brindled was active in about 60% of cells, while in the Low line it was active in about 25% of cells. The whole of the difference was caused by the chromosomes carrying brindled: neither the unmarked X chromosome nor the autosomes were differentiated. There was a positive correlation between the expression of brindled in daughters and mothers. This was probably not caused by residual genetic variation, but was more probably a maternal effect similar to that described by Cattanach & Papworth (1981). On this assumption the daughters' scores were adjusted to a standard maternal score. Enzyme assays on females doubly heterozygous for brindled and for the sex-linked Pgk-1 locus proved that the percentage of brindled in the coat provided an accurate measure of the X-inactivation proportions in the blood, liver and kidney. The accuracy was improved by adjustment for maternal score. In the selection lines, brindled was always inherited from the mother. When brindled was transmitted by male parents the probability of activation of its chromosome was increased by 8 percentage points in the High line and 18 in the Low line. This effect of the parental source is much greater than has previously been reported. The responses to selection can be interpreted in terms of the Xce locus controlling the activation probability, different alleles on the chromosomes carrying brindled being selected in the two lines. If this interpretation is correct, the alleles on one or both of the chromosomes carrying brindled were different from any of the three known alleles. The different effects of male transmission in the two lines can be described as a difference between the two chromosomes in their reactions to imprinting. This difference might possibly also be due to the Xce locus.

Type
Research Article
Information
Genetics Research , Volume 39 , Issue 3 , June 1982 , pp. 237 - 259
Copyright
Copyright © Cambridge University Press 1982

References

REFERENCES

Beutler, E. (1969). Electrophoresis of phosphoglycerate kinase. Biochemical Genetics 3, 189–195.CrossRefGoogle ScholarPubMed
Cattanach, B. M. (1975). Control of chromosome inactivation. Annual Review of Genetics 9, 1–18.CrossRefGoogle ScholarPubMed
Cattanach, B. M. & Isaacson, J. H. (1965). Genetic control over the inactivation of autosomal genes attached to the X-chromosomes. Zeitschrift für inductive Abstammungs- und Verer-bungslehre 96, 313–323.Google Scholar
Cattanach, B. M. & Isaacson, J. H. (1967). Controlling elements in the mouse X chromosome. Genetics 57, 331–346.CrossRefGoogle ScholarPubMed
Cattanach, B. M. & Papworth, D. (1981). Controlling elements in the mouse. V. Linkage tests with X-linked genes. Genetical Research 38, 57–70.CrossRefGoogle ScholarPubMed
Cattanach, B. M. & Perez, J. N. (1970). Parental influence on X-autosome translocation induced variegation in the mouse. Genetical Research 15, 43–53.CrossRefGoogle ScholarPubMed
Chandra, H. S. & Brown, S. W. (1975). Chromosome imprinting and the mammalian X chromosome. Nature 253, 165–168.CrossRefGoogle ScholarPubMed
Falconer, D. S., Gauld, I. K., Roberts, R. C. & Williams, D. A. (1981). The control of body size in mouse chimaeras. Genetical Research 38, 25–46.CrossRefGoogle ScholarPubMed
Falconer, D. S. & Isaacson, J. H. (1972). Sex-linked variegation modified by selection in brindled mice. Genetical Research 20, 291–316.CrossRefGoogle ScholarPubMed
Hunt, D. M. (1974). Primary defect in copper transport underlies mottled mutants in the mouse. Nature 249, 852–854.CrossRefGoogle ScholarPubMed
Hunt, D. M. (1976). A study of copper treatment and tissue copper levels in the murine congenital copper deficiency, mottled. Life Sciences 19, 1913–1920.CrossRefGoogle ScholarPubMed
Johnston, P. G. & Cattanach, B. M. (1981). Controlling elements in the mouse. IV. Evidence of non-random X-inactivation. Genetical Research 37, 151–160.CrossRefGoogle ScholarPubMed
Klebe, R. J. (1975). A simple method for the quantitation of isozyme patterns. Biochemical Genetics 13, 805–812.CrossRefGoogle ScholarPubMed
Lyon, M. F. (1961). Gene action in the X-chromosome of the mouse (Mus musculus L.). Nature 190, 372–373.CrossRefGoogle ScholarPubMed
Nesbitt, M. N. (1971). X chromosome inactivation mosaicism in the mouse. Developmental Biology 26, 252–263.CrossRefGoogle Scholar
Nielsen, J. T. & Chapman, V. M. (1977). Electrophoretic variation for sex-linked phospho-glycerate kinase (PGK-1) in the mouse. Genetics 87, 319–325.CrossRefGoogle Scholar
Papaioannou, V. E. & West, J. D. (1981). Relationship between the parental origin of the X chromosome, embryonic cell lineage and X chromosome expression in mice. Genetical Research 37, 183–197.CrossRefGoogle Scholar
Sharman, G. B. (1971). Late DNA replication in the paternally derived X chromosome of female kangaroos. Nature 230, 231–232.CrossRefGoogle ScholarPubMed
West, J. D. & Chapman, V. M. (1978). Variation for X chromosome expression in mice detected by electrophoresis of phosphoglycerate kinase. Genetical Research 32, 91–102.CrossRefGoogle ScholarPubMed