Non-additive inheritance of glucose phosphate isomerase activity in mice heterozygous at theGpi-1sstructural locus

Abstract

SummaryThe activity of blood glucose phosphate isomerase (GPI-1) in mice heterozygous for various alleles at theGpi-1sstructural locus (heterozygotesa/b, a/candb/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 ina/bheterozygotes 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 stabilitiesin vivowould 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.