International Mammalian Genome Society

The 15th International Mouse Genome Conference (2001)


Dr. Fernando Pardo-Manuel de Villena
The University of North Carolina at Chapel Hill
Department of Genetics CB # 7264
102 Mason Farm Road
Chapel Hill, NC 27599-7264

Co-Authors: 1)Bell, TA, 2)Briscoe TL, 2)Sapienza C
Institutions: 1)Department of Genetics, University of North Carolina at Chapel Hill 2)Fels Institute for Cancer Research and Molecular Biology. Temple University School of Medicine

Crosses between heterozygous females for DDK alleles at the Om locus and males from many inbred strains show two striking phenotypes, embryonic lethality and maternal transmission ratio distortion (TRD). We have shown previously that TRD is due to nonrandom segregation at the second meiotic division. This conclusion was based in the demonstration that meiotic recombination between Om and the centromere has a significant effect on the level of distortion. However, some doubt remained due to the fact that distortion was dependent upon the genotype of the sire. Offspring of B6 males show distortion while the progeny of DDK males follow Mendelian ratios. Lastly, the segregation of alleles in intercrosses indicates that the sire effect segregate as a single locus linked to Om with haploid gene action. To test the validity of our conclusion we have characterized the DDK syndrome and TRD phenotypes in the offspring of males with mixed B6/DDK genetic backgrounds. As expected, the lethality shows a perfect correlation with the sire genotype at Om. In contrast, the TRD is unrelated to the genotype of the sire at Om, i. e., the lethality is unrelated to TRD. For example, there is TRD (P<0.0001) in 1388 offspring of crosses with no lethality. We conclude that the distortion is due to nonrandom segregation and that the sperm is able to interact with female meiotic apparatus. This experiment allows us to define a candidate interval for the effect of the sperm.

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