BALB/c Alleles at Modifier Loci Increase the Severity of the Maternal Effect of the "DDK Syndrome"

Corresponding author: Patricia Baldacci, Unité de Biologie du Développement, Département d'Immunologie, Institut Pasteur, 25, rue du Dr Roux, 75724 Paris Cedex 15, France., baldacci{at}pasteur.fr (E-mail)

Communicating editor: D. M. KINGSLEY

The Om locus was first described in the DDK inbred mouse strain: DDK mice carry a mutation at Om resulting in a parental effect lethality of F₁ embryos. When DDK females are mated with males of other (non-DDK) inbred strains, e.g., BALB/c, they exhibit a low fertility, whereas the reciprocal cross, non-DDK females x DDK males, is fertile (as is the DDK intrastrain cross). The low fertility is due to the death of (DDK x non-DDK)F₁ embryos at the late-morula to blastocyst stage, which is referred to as the "DDK syndrome." The death of these F₁ embryos is caused by an incompatibility between a DDK maternal factor and the non-DDK paternal pronucleus. Previous genetic studies showed that F₁ mice have an intermediate phenotype compared to parental strains: crosses between F₁ females and non-DDK males are semisterile, as are crosses between DDK females and F₁ males. In the present studies, we have examined the properties of mice heterozygous for BALB/c and DDK Om alleles on an essentially BALB/c genetic background. Surprisingly, we found that the females are quasi-sterile when mated with BALB/c males and, thus, present a phenotype similar to DDK females. These results indicate that BALB/c alleles at modifier loci increase the severity of the DDK syndrome.

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