Migration restores hybrid incompatibility driven by mitochondrial-nuclear sexual conflict

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 compe...

Full description

Saved in:
Bibliographic Details
Published in:Proceedings of the Royal Society. B, Biological sciences Biological sciences, 2022-01, Vol.289 (1967), p.20212561-20212561
Main Authors: Munasinghe, Manisha, Haller, Benjamin C, Clark, Andrew G
Format: Article
Language:English
Subjects:
Cell Nucleus - genetics
Evolution
Female
Genome, Mitochondrial
Humans
Male
Mitochondria - genetics
Mutation
Reproductive Isolation
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary: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.
ISSN:0962-8452
1471-2954
DOI:10.1098/rspb.2021.2561