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Genetics, Vol. 170, 327-334, May 2005, Copyright © 2005
doi:10.1534/genetics.104.039479
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,3
* Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, Philadelphia, Pennsylvania 19140
Department of Pathology and Laboratory Medicine, Temple University School of Medicine, Philadelphia, Pennsylvania 19140
Department of Biochemistry, Temple University School of Medicine, Philadelphia, Pennsylvania 19140
Department of Genetics, Lineberger Comprehensive Cancer Center, Carolina Center for Genome Sciences, University of North Carolina, Chapel Hill, North Carolina 27599-7264
3 Corresponding author: Fels Institute for Cancer Research and Molecular Biology, Temple University School of Medicine, 3307 N. Broad St., Philadelphia, PA 19140.
E-mail: sapienza{at}temple.edu
50%), differences in the level of TRD found in recombinant vs. nonrecombinant chromosomes among offspring argue that TRD is due to nonrandom segregation of chromatids at the second meiotic division, i.e., true meiotic drive. We tested this hypothesis directly, by determining the centromere and Om genotypes of individual chromatids in zygote stage embryos. We found similar levels of TRD in favor of DDK alleles at Om in the female pronucleus and TRD in favor of C57BL/6 alleles at Om in the second polar body. In those embryos for which complete dyads have been reconstructed, TRD was present only in those inheriting heteromorphic dyads. These results demonstrate that meiotic drive occurs at MII and that preferential death of one genotypic class of embryo does not play a large role in the TRD. This article has been cited by other articles:
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