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Modification of Survival Rate of Mouse Embryos Developing in Heterozygous Females for Ovum Mutant Gene¹

^a Laboratory of Animal Reproduction, Graduate School of Bioagricultural Sciences, Nagoya University, Chikusa, Nagoya, Aichi, 464–8601, Japan

The DDK syndrome (polar infertility) is caused by an incompatibility system due to the ovum mutant (Om) locus. For brevity, the following gene symbols are used in the present report: DDK allele, Om; C57BL/6Cr allele, +. In this investigation, we first attempted to introduce the Om allele of DDK strain into the genetic background of C57BL/6Cr strain. The attempt resulted in the production of no young at the third generation of successive backcrosses. Secondly, mating experiments were performed with heterozygous (Om/+) females having background genes of C57BL/6Cr and DDK strains in the ratios 1:1(B1D), 3:1(B3D), 7:1(B7D), and 15:1(B15D). The survival rate of the embryos as judged by the percentage number of live fetuses/number of corpora lutea at Day 12 of pregnancy was 41.3 ± 3.2%, 27.3 ± 3.2%, 16.4 ± 3.3%, and 11.3 ± 3.2% (mean ± SEM) in the B1D, B3D, B7D, and B15D females, respectively, when they were mated with C57BL/6Cr males. Furthermore, the increased embryonic mortality in the heterozygous (Om/+) females with more background genes of C57BL/6Cr strain was found to be due to a failure in blastocyst formation, as in the DDK syndrome. The parallelism between the proportion of C57BL/6Cr background genes and embryonic mortality has led to a hypothesis proposing the participation of a modifier gene, namely that a mechanism similar to allelic exclusion may be working in the synthesis of cytoplasmic factor of eggs and that only the Om allele is activated during oogenesis to produce DDK-type cytoplasmic factor in heterozygous (Om/+) females having a modifier gene in the homozygous state.

First decision: 9 August 1999.

¹ This work was supported in part by a grant-in-aid for scientific research to N.W. from the Ministry of Education, Science, Sports and Culture of Japan (No. 05304022).

² Correspondence. FAX: 81 52 789 4012; w16341a{at}nuagr1.agr.nagoya-u.ac.jp

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