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Genetics. 2011 Nov;189(3):1001-9. doi: 10.1534/genetics.111.132324. Epub 2011 Sep 6.

Genetic architecture of male sterility and segregation distortion in Drosophila pseudoobscura Bogota-USA hybrids.

Author information

1
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109, USA. nitin@fhcrc.org

Abstract

Understanding the genetic basis of reproductive isolation between recently diverged species is a central problem in evolutionary genetics. Here, I present analyses of the genetic architecture underlying hybrid male sterility and segregation distortion between the Bogota and USA subspecies of Drosophila pseudoobscura. Previously, a single gene, Overdrive (Ovd), was shown to be necessary but not sufficient for both male sterility and segregation distortion in F(1) hybrids between these subspecies, requiring several interacting partner loci for full manifestation of hybrid phenomena. I map these partner loci separately on the Bogota X chromosome and USA autosomes using a combination of different mapping strategies. I find that hybrid sterility involves a single hybrid incompatibility of at least seven interacting partner genes that includes three large-effect loci. Segregation distortion involves three loci on the Bogota X chromosome and one locus on the autosomes. The genetic bases of hybrid sterility and segregation distortion are at least partially--but not completely--overlapping. My results lay the foundation for fine-mapping experiments to identify the complete set of genes that interact with Overdrive. While individual genes that cause hybrid sterility or inviability have been identified in a few cases, my analysis provides a comprehensive look at the genetic architecture of all components of a hybrid incompatibility underlying F(1) hybrid sterility. Such an analysis would likely be unfeasible for most species pairs due to their divergence time and emphasizes the importance of young species pairs such as the D. pseudoobscura subspecies studied here.

PMID:
21900263
PMCID:
PMC3213365
DOI:
10.1534/genetics.111.132324
[Indexed for MEDLINE]
Free PMC Article

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