Abstract
Resolving the mechanistic and genetic bases of reproductive barriers between species is essential to understanding the evolutionary forces that shape speciation. Intrinsic hybrid incompatibilities are often treated as fixed between species, yet there can be considerable variation in the strength of reproductive isolation between populations. The extent and causes of this variation remain poorly understood in most systems. We investigated the genetic basis of variable hybrid male sterility (HMS) between two recently diverged subspecies of house mice, Mus musculus domesticus and Mus musculus musculus. We found that polymorphic HMS has a surprisingly complex genetic basis, with contributions from at least five autosomal loci segregating between two closely related wild-derived strains of M. m. musculus. One of the HMS-linked regions on chromosome 4 also showed extensive introgression among inbred laboratory strains and transmission ratio distortion (TRD) in hybrid crosses. Using additional crosses and whole genome sequencing of sperm pools, we showed that TRD was limited to hybrid crosses and was not due to differences in sperm motility between M. m. musculus strains. Based on these results, we argue that TRD likely reflects additional incompatibilities that reduce hybrid embryonic viability. In some common inbred strains of mice, selection against deleterious interactions appears to have unexpectedly driven introgression at loci involved in epistatic hybrid incompatibilities. The highly variable genetic basis to F1 hybrid incompatibilities between closely related mouse lineages argues that a thorough dissection of reproductive isolation will require much more extensive sampling of natural variation than has been commonly utilized in mice and other model systems.
| Original language | English |
|---|---|
| Pages (from-to) | 845-859 |
| Number of pages | 15 |
| Journal | Genetics |
| Volume | 209 |
| Issue number | 3 |
| DOIs | |
| State | Published - Jul 2018 |
Funding
We thank Kathleen Tsung, Joseph Dysthe, Brent Young, Nick Schultz, Selene Tyndale, and Charlie Nicolet for assistance with data collection and analysis. We also thank members of the Good laboratory; Ryan Bracewell, Lila Fishman, David Aylor, Bret Payseur, Michael Nachman, Peter Ellis, and two anonymous reviewers for helpful feedback; the Vincent J. Coates Genomics Sequencing Laboratory at the University of California Berkeley, supported by the National Institutes of Health S10 instrumentation grants S10RR029668 and S10RR027303; and the University of Montana Genomics Core, supported by a grant from the M.J. Murdock Charitable Trust. This research was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health (R01-HD073439 and R01-HD094787 to J.M.G.), the National Institute of General Medical Sciences (R01-GM098536 to M.D.D.), and the National Science Foundation (1146525 to M.D.D.). Author contributions: J.M.G. conceived the study. J.M.G., E.L.L., and M.D.D. designed the experiments. E.L.L., D.V., C.C., V.S., E.N., and L.P.P. performed experiments and collected data. E.L.L., D.V., B.A.J.S., S.K., L.P.P., M.D.K., and M.D.D. analyzed data. E.L.L. and J.M.G. wrote the manuscript with feedback from the authors. We thank Kathleen Tsung, Joseph Dysthe, Brent Young, Nick Schultz, Selene Tyndale, and Charlie Nicolet for assistance with data collection and analysis. We also thank members of the Good laboratory; Ryan Bracewell, Lila Fishman, David Aylor, Bret Payseur, Michael Nachman, Peter Ellis, and two anonymous reviewers for helpful feedback; the Vincent J. Coates Genomics Sequencing Laboratory at the University of California Berkeley, supported by the National Institutes of Health S10 instrumentation grants S10RR029668 and S10RR027303; and the University of Montana Genomics Core, supported by a grant from the M.J. Murdock Charitable Trust. This research was supported by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the National Institutes of Health (R01-HD073439 and R01-HD094787 to J.M.G.), the National Institute of General Medical Sciences (R01-GM098536 to M.D.D.), and the National Science Foundation (1146525 to M.D.D.).
| Funders | Funder number |
|---|---|
| 1146525 | |
| S10RR027303, S10RR029668 | |
| R01-GM098536 | |
| R01HD073439 | |
| University of California at Berkeley | |
| R01-HD094787 |
Keywords
- Hybrid male sterility
- Introgression
- Polymorphism
- QTL mapping
- Transmission ratio distortion
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