The paramount importance of an early single endosymbiotic event in the origin of the eukaryotic cell is now well appreciated among biologists. What is much less appreciated is how the mitochondrial endosymbiont has shaped the evolution of cellular and genomic features of eukaryotic lineages. Mitochondrial variation in natural populations has been traditionally considered as essentially neutral and, accordingly, used during the last two decades to reconstruct the phylogenetic history of maternal lineages in a huge number of animal and plant species. However, there is increasing evidence from different organisms for extensive mitonuclear epistasis in fitness-related traits, as well as for selective sweeps that can apparently drive mitochondrial haplotypes to fixation throughout large geographic regions. Strikingly discordant phylogeographic patterns of nuclear and mitochondrial markers within animal species are repeatedly explained by ever more cumbersome "ad-hoc" explanations, pivoting around sex-biased dispersal, germ-line infections and the smaller effective size of the mitochondrial gene pool, disregarding their most likely cause, namely the evolution of cytonuclear Dobzhansky- Muller (D-M) incompatibilities. Direct evidence of mitonuclear incompatibilities in wild populations is relatively common in plants, where they may have played a major role in the evolution of angiosperms, but it is still scarce in animals. The necessity to keep pace with mitochondrial mutation accumulation is also of utmost importance for our own species, due to the pathogenic effects of many of those mutations, which can be compensated by nuclear modifiers of the mitochondrial function. The vast amount of available genomic data offers an unprecedented opportunity to assess the impact of cytonuclear coevolution on human disease.
Besides mitochondria, other endosymbionts of bacterial, archaeal and fungal origin have been documented in the eukaryotic cytoplasm. As a result, the nuclear genome does not just coevolve with its mitochondrial counterpart, but also with other intracellular genomes, thus providing new sources of intergenomic conflict and new opportunities for speciation. The results of these studies are clearly relevant to our understanding of the role of endosymbiosis in the evolution of eukaryotic organisms.
This Research Topic is an effort to assess the role of cytonuclear conflict as an engine of speciation.
This Research Topic welcomes original research papers, reviews and new ideas related, but not limited, to the following topics:
- Role of cytonuclear incompatibilities in shaping cellular and genomic architectures, as well as supracellular organization.
- Revisions of evolutionary histories of populations based on phylogeographic patterns of mitochondrial markers.
- Genetic and molecular analyses of cytonuclear epistasis.
- Gametic disequilibria of nuclear and cytoplasmic haplotypes from contact regions.
- Interactions between coexisting intracellular genomes.
- Contributions of cytonuclear incompatibilities to reproductive barriers between populations or species.
- Standing genetic variation of nuclear modifiers of mitochondrial function.
- Cytonuclear coevolution and human disease.
The paramount importance of an early single endosymbiotic event in the origin of the eukaryotic cell is now well appreciated among biologists. What is much less appreciated is how the mitochondrial endosymbiont has shaped the evolution of cellular and genomic features of eukaryotic lineages. Mitochondrial variation in natural populations has been traditionally considered as essentially neutral and, accordingly, used during the last two decades to reconstruct the phylogenetic history of maternal lineages in a huge number of animal and plant species. However, there is increasing evidence from different organisms for extensive mitonuclear epistasis in fitness-related traits, as well as for selective sweeps that can apparently drive mitochondrial haplotypes to fixation throughout large geographic regions. Strikingly discordant phylogeographic patterns of nuclear and mitochondrial markers within animal species are repeatedly explained by ever more cumbersome "ad-hoc" explanations, pivoting around sex-biased dispersal, germ-line infections and the smaller effective size of the mitochondrial gene pool, disregarding their most likely cause, namely the evolution of cytonuclear Dobzhansky- Muller (D-M) incompatibilities. Direct evidence of mitonuclear incompatibilities in wild populations is relatively common in plants, where they may have played a major role in the evolution of angiosperms, but it is still scarce in animals. The necessity to keep pace with mitochondrial mutation accumulation is also of utmost importance for our own species, due to the pathogenic effects of many of those mutations, which can be compensated by nuclear modifiers of the mitochondrial function. The vast amount of available genomic data offers an unprecedented opportunity to assess the impact of cytonuclear coevolution on human disease.
Besides mitochondria, other endosymbionts of bacterial, archaeal and fungal origin have been documented in the eukaryotic cytoplasm. As a result, the nuclear genome does not just coevolve with its mitochondrial counterpart, but also with other intracellular genomes, thus providing new sources of intergenomic conflict and new opportunities for speciation. The results of these studies are clearly relevant to our understanding of the role of endosymbiosis in the evolution of eukaryotic organisms.
This Research Topic is an effort to assess the role of cytonuclear conflict as an engine of speciation.
This Research Topic welcomes original research papers, reviews and new ideas related, but not limited, to the following topics:
- Role of cytonuclear incompatibilities in shaping cellular and genomic architectures, as well as supracellular organization.
- Revisions of evolutionary histories of populations based on phylogeographic patterns of mitochondrial markers.
- Genetic and molecular analyses of cytonuclear epistasis.
- Gametic disequilibria of nuclear and cytoplasmic haplotypes from contact regions.
- Interactions between coexisting intracellular genomes.
- Contributions of cytonuclear incompatibilities to reproductive barriers between populations or species.
- Standing genetic variation of nuclear modifiers of mitochondrial function.
- Cytonuclear coevolution and human disease.