An essential cell cycle regulation gene causes hybrid inviability in Drosophila
Essential genes and species incompatibilities
Crosses between two fruit fly species, Drosophila melanogaster and D. simulans, result in hybrid progeny that are all female. Although some of the genes responsible for this species barrier are known, the full complement of molecular determinants that lead to inviable males has remained mysterious. Phadnis et al. used mutagenesis and a sequencing-based genomic screen to link hybrid inviability to the cell cycle. The inviable males result from an interaction between three genes, one of which is essential, which precluded its identification with standard genetic screens. This strategy to identify speciation genes can be applied to other model and nonmodel systems.
Science, this issue p. 1552
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.
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Supplementary Material
Summary
Materials and Methods
Tables S1 to S4
Figs. S1 to S12
Resources
File (aac7504_phadnis_sm.pdf)
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Information & Authors
Information
Published In
Science
Volume 350 | Issue 6267
18 December 2015
18 December 2015
Copyright
Copyright © 2015, American Association for the Advancement of Science.
Submission history
Received: 8 June 2015
Accepted: 13 November 2015
Published in print: 18 December 2015
Acknowledgments
We thank T. Levin, M. Levine, M. Patel, Naina Phadnis, B. Ross, and S. Zanders for their comments on the manuscript and members of the Malik, Peichel, and Phadnis labs for discussions. This work was supported by a Howard Hughes Medical Institute–Life Sciences Research Foundation (HHMI-LSRF) postdoctoral fellowship (N.P.); a Mario Cappecchi–endowed assistant professorship (N.P.); an NIH Developmental Biology Training Grant 5T32 HD0741 (J.C.C.); graduate research fellowship DGE-071824 from the NSF (J.O.K.); grants from the NIH: R01 GM115914 (N.P.), HG006283 (J.S.), and R01 GM074108 (H.S.M.); and especially a grant from the Mathers Foundation (H.S.M.). J.S. and H.S.M. are investigators of HHMI. The data reported in this paper are tabulated in the supplementary materials and archived at the following databases: primary read data at the Sequence Read Archive under accession number PRJNA290665 and gfzf sequences at GenBank under accession numbers KU064780 to KU064795.
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