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doi:10.1534/genetics.105.053272
A more recent version of this article appeared on June 1, 2006.
REGULAR RESEARCH PAPERS |
A Genetic Test of the Role of the Maternal Pronucleus in Wolbachia-Induced Cytoplasmic Incompatibility
Patrick M Ferree 1* and William Sullivan 1
1 University of California, Santa Cruz
* To whom correspondence should be addressed. E-mail: ferree{at}biology.ucsc.edu.
Submitted on November 8, 2005
Revised on December 20, 2005
Accepted on 6 April 2006
Cytoplasmic Incompatibility (CI) is a reproductive sterility found in Arthropods that is caused by the endoparasitic bacteria Wolbachia. In CI, host progeny fail to develop during early embryogenesis if Wolbachia-infected males fertilize uninfected females. It is widely accepted that this lethality is caused by some unknown Wolbachia-induced modification of the paternal nuclear material in the host testes. However, the direct means by which this modification leads to early embryonic death is currently unresolved. Results from previous studies suggested that CI lethality occurs as a result of asynchrony in cell cycle timing between the paternal and maternal pronuclei. This hypothesis can be tested experimentally by the prediction that the Wolbachia-modified paternal pronucleus should support androgenetic development (i.e., from the paternal pronucleus only). Using specific mutations in Drosophila melanogaster that produce androgenetic progeny, we demonstrate that the Wolbachia-induced modification inhibits this type of development. This result suggests that CI occurs independently of the maternal pronucleus and argues against pronuclear asynchrony as the primary cause of CI lethality. We propose that CI occurs instead as the result of either a developmentally incompetent paternal pronucleus or asynchrony between the paternal pronucleus and the cell cycle of the egg cytoplasm.
Key Words: Wolbachia, Cytoplasmic Incompatibility (CI), androgenesis, checkpoints, pronucleus
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