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Non-additive inheritance of glucose phosphate isomerase activity in mice heterozygous at the Gpi-1s structural locus

Published online by Cambridge University Press:  14 April 2009

John D. West  and
Jean H. Flockhart
John D. West
Affiliation:
Department of Obstetrics and Gynaecology, University of Edinburgh, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9EW
Jean H. Flockhart
Affiliation:
Department of Obstetrics and Gynaecology, University of Edinburgh, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9EW
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The activity of blood glucose phosphate isomerase (GPI-1) in mice heterozygous for various alleles at the Gpi-1s structural locus (heterozygotes a/b, a/c and b/c) was significantly higher than expected, on the basis of additive inheritance, from the levels in parental homozygotes. Moreover, the GPI-1 activity was higher in a/b heterozygotes than in either parent (heterosis). Studies of heat stability with kidney homogenates revealed that the relative stabilities of GPI-1 dimers was AA > AB > BB > AC ≥ BC > CC. Differences in dimer stabilities in vivo would affect the total GPI-1 levels in heterozygotes and could account for non-additive inheritance but would be insufficient to explain heterosis for GPI-1 activity. Other possible contributing factors include unequal production or stability of monomers, or higher catalytic activity of heterodimers. Monomers could also associate non-randomly but this would not be sufficient to explain heterosis. It is clear that non-additive inheritance patterns may be produced by variants of either structural or regulatory genes.

Type
Research Article
Information
Genetics Research , Volume 54 , Issue 1 , August 1989 , pp. 27 - 36
Copyright
Copyright © Cambridge University Press 1989

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