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Genetics, Vol 143, 1629-1642, Copyright © 1996
INVESTIGATIONS |
A. F. Dernburg, D. R. Daily, K. J. Yook, J. A. Corbin, J. W. Sedat and W. Sullivan
Department of Biochemistry and Biophysics, University of California, San Francisco, California 94143-0554 Present address: Department of Developmental Biology, Stanford University School of Medicine, B309 Beckman Center, Stanford, CA 94305. These two authors contributed equally.
The Drosophila compound entire second chromosome, C(2)EN, displays paternal transmission well below Mendelian expectations (NOVITSKI et al. 1981). Because C(2)EN stocks also show higher-than-expected rates of zygotic lethality, it was proposed that this reduced paternal inheritance might be wholly or partially due to postfertilization events. Efforts to investigate this phenomenon have been hampered because the progeny of crosses between C(2)EN-bearing individuals and those with normal karyotypes die during embryogenesis. We have circumvented this obstacle by employing fluorescence in situ hybridization to directly karyotype early embryos from crosses involving C(2)EN-bearing individuals. This analysis reveals that the distortion in paternal transmission is established before fertilization. Moreover, measurement of the sperm ratios within both the male and female reproductive organs demonstrates that C(2)EN-bearing sperm are selectively lost after sperm transfer to the female and before storage of sperm in the seminal receptacles and spermathecae. Our results are consistent with a model of meiotic drive in which aberrations occuring early in meiosis lead ultimately to sperm dysfunction.
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