ArticleProceedings. Biological sciences2022
Migration restores hybrid incompatibility driven by mitochondrial-nuclear sexual conflict.
Article in Proceedings. Biological sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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4 citing papers in PubMed, 6 citations in OpenAlex.
- SLiM 5: Eco-evolutionary Simulations Across Multiple Chromosomes and Full Genomes.Molecular biology and evolution · 2026Article
- A genomic test of sex-biased dispersal in white sharks.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Unravelling the role of mitochondrial DNA in hybrid incompatibility within species of the Anopheles gambiae complex.Scientific reports · 2024Article
- Mother's Curse effects on lifespan and aging.Frontiers in aging · 2024Review
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Authors and funding
3 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
In the mitochondrial genome, sexual asymmetry in transmission allows the accumulation of male-harming mutations since selection acts only on the effect of the mutation in females. Called the 'Mother's Curse', this phenomenon induces a selective pressure for nuclear variants that compensate for this reduction in male fitness. Previous work has demonstrated the existence of these interactions and their potential to act as Dobzhansky-Muller incompatibilities, contributing to reproductive isolation between populations. However, it is not clear how readily they would give rise to and sustain hybrid incompatibilities. Here, we use computer simulations in SLiM 3 to investigate the consequences of sexually antagonistic mitochondrial-nuclear interactions in a subdivided population. We consider distinct migration schemes and vary the chromosomal location, and consequently the transmission pattern, of nuclear restorers. Disrupting these co-evolved interactions results in less-fit males, skewing the sex ratio toward females. Restoration of male fitness depends on both the chromosomal location of nuclear restorer loci and the migration scheme. Our results show that these interactions may act as Dobzhansky-Muller incompatibilities, but their strength is not enough to drive population isolation. Overall, this model shows the varied ways in which populations can respond to migration's disruption of co-evolved mitochondrial-nuclear interactions.
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