International Mammalian Genome Society

logo18th International Mouse Genome Conference

17-22 October 2004, Seattle, USA


POSTER 38 - MODIFIERS OF THE DDK SYNDROME RESULT IN THE DOMINANT RESCUE OF EMBRYONIC LETHALITY

Ideraabdullah FY, Kim K, Pardo-Manuel de Villena F

Dept of Genetics, UNC-Chapel Hill, Chapel Hill, United States

The DDK syndrome is an early embryonic lethal phenotype that is observed in crosses involving females of the DDK inbred strain and males of other strains. This phenotype is the result of an incompatibility between a maternal DDK factor and a non-DDK paternal gene, both of which have been mapped to the Ovum mutant (Om) locus on mouse chromosome 11. Previous studies have shown that F1 hybrid females resulting from crosses involving a non-DDK dam and a DDK sire, express a semi-lethal phenotype when crossed to B6 males. It has been suggested that the semi-lethal nature of the phenotype in these females is the result of allelic exclusion acting on the Om  locus. In this study, we tested the fertility of several F1 hybrid  females derived from crossing females of classical or wild-derived strains with DDK males.  Although most of the crosses are semi-lethal, two crosses involving F1 females from wild-derived Mus musculus domesticus strains, PERA/Ei or PERC/Ei, are viable. Our observations indicate the presence of genetic modifiers of the DDK syndrome that result in dominant rescue of lethality. Further investigation revealed that the PERA/Ei and PERC/Ei modifiers segregate independently of the Om locus.  We hypothesize that these dominant modifiers skew expression of the maternal factor in favor of the non-DDK allele at Om, by means of allelic exclusion. Currently, efforts are being made to identify these modifiers by genome scan and characterize their role in allelic exclusion.

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