Inheritance of a meiotic abnormality that causes the ovulation of primary oocytes and the production of digynic triploid mice.

Previous studies have demonstrated that the LT/SvKau strain of mice ovulates a high proportion of oocytes as diploid primary oocytes rather than secondary oocytes. These ovulated primary oocytes are arrested at meiotic metaphase I but may be fertilized to produce digynic triploid embryos. In the present study, 40.4% of eggs analysed from LT/SvKau females were ovulated as primary oocytes, compared to 1.2% from control C57BL/Ws strain mothers. These two inbred strains were intercrossed to produce eight sets of F1, F2 and backcross females and the frequency of triploidy was investigated. The results are compatible with segregation of a co-dominant, autosomal gene that has a major influence on the incidence of triploidy. We suggest that the provisional gene symbol Poo (primary oocyte ovulation) be assigned to this gene, with alleles Poo(l) (the 'mutant' allele present in the LT/SvKau strain) and Poo(b) (the normal allele present in C57BL/Ws mice). Poo is incompletely penetrant and has variable expressivity because the proportion of oocytes ovulated as primary oocytes by LT/SvKau mice was variable and, in some cases, nil. In putative Poo(l)/Poo(b) heterozygotes the frequency of ovulated primary oocytes was increased only marginally (from 1.2% to 6.6%) by the presence of one copy of the Poo(l) allele, but this increase was found consistently (in two reciprocal F1 crosses) and was statistically significant. No evidence was found for tight genetic linkage between Poo and two Mendelian loci (brown on chromosome 4 and glucose phosphate isomerase on chromosome 7), that were segregating in the crosses. The Poo(l) mutant in the LT/SvKau strain of mice provides a valuable resource to study the cell and molecular biology of mammalian oocyte maturation and the control of meiosis.