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Science. 2015 Dec 18;350(6267):1552-5. doi: 10.1126/science.aac7504.

An essential cell cycle regulation gene causes hybrid inviability in Drosophila.

Author information

1
Department of Biology, University of Utah, Salt Lake City, UT 84112, USA. nitin.phadnis@utah.edu hsmalik@fhcrc.org.
2
Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA.
3
Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.
4
Genome Sciences, University of Washington, Seattle, WA 98195, USA. Howard Hughes Medical Institute, University of Washington, Seattle, WA 98195, USA.
5
Genome Sciences, University of Washington, Seattle, WA 98195, USA. Department of Human Genetics, University of Michigan, Ann Arbor, MI 48109, USA.
6
Basic Sciences Division, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. Howard Hughes Medical Institute, Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA. nitin.phadnis@utah.edu hsmalik@fhcrc.org.

Abstract

Speciation, the process by which new biological species arise, involves the evolution of reproductive barriers, such as hybrid sterility or inviability between populations. However, identifying hybrid incompatibility genes remains a key obstacle in understanding the molecular basis of reproductive isolation. We devised a genomic screen, which identified a cell cycle-regulation gene as the cause of male inviability in hybrids resulting from a cross between Drosophila melanogaster and D. simulans. Ablation of the D. simulans allele of this gene is sufficient to rescue the adult viability of hybrid males. This dominantly acting cell cycle regulator causes mitotic arrest and, thereby, inviability of male hybrid larvae. Our genomic method provides a facile means to accelerate the identification of hybrid incompatibility genes in other model and nonmodel systems.

PMID:
26680200
PMCID:
PMC4703311
DOI:
10.1126/science.aac7504
[Indexed for MEDLINE]
Free PMC Article

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