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The DNA transposition system of hybrid dysgenesis in Drosophila melanogaster can function despite defects in host DNA repair

Published online by Cambridge University Press:  14 April 2009

Barton E. Slatko ,
James M. Mason  and
R. C. Woodruff
Barton E. Slatko*
Affiliation:
Department of Biology, Williams College, Williamstown, Massachusetts, USA01267
James M. Mason
Affiliation:
National Institute of Environmental Health Sciences, P.O. Box 12233, Research Triangle Park, North Carolina, USA27709
R. C. Woodruff
Affiliation:
Department of Biological Sciences, Bowling Green University, Bowling Green, Ohio, USA43403
*
* To whom proofs and correspondence should be addressed.
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Summary

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Genetic traits associated with the hybrid dysgenesis syndrome were quantified in strains deficient in two major host-coded DNA repair pathways, post-replication and excision repair. A defect in either (or both) pathway(s) fails to influence the frequency of male recombination or sex-linked recessive lethal mutations associated with hybrid dysgenesis, suggesting that the DNA transposable elements associated with this syndrome act independently of these cellular functions. However, when the post-replication repair pathway is blocked, the recovery of second chromosomes containing factors associated with hybrid dysgenesis activity is reduced. The decrease in recovery is associated with zygotic lethality.

Type
Research Article
Information
Genetics Research , Volume 43 , Issue 2 , April 1984 , pp. 159 - 171
Copyright
Copyright © Cambridge University Press 1984

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