ORCID Profile
0000-0002-6824-1674
Current Organisations
University of Sydney
,
University of Zurich
,
University of Pennsylvania
,
University College London
,
Wissenschaftskolleg zu Berlin eV
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Publisher: Cold Spring Harbor Laboratory
Date: 13-02-2021
DOI: 10.1101/2021.02.12.430938
Abstract: Across eukaryotes, genes encoding bioenergetic machinery are located in both mitochondrial and nuclear DNA, and incompatibilities between the two genomes can be devastating. Mitochondria are often inherited maternally, and theory predicts sex-specific fitness effects of mitochondrial mutational ersity. Yet how evolution acts on linkage patterns between mitochondrial and nuclear genomes is poorly understood. Using novel mito-nuclear population genetic models, we show that the interplay between nuclear and mitochondrial genes maintains mitochondrial haplotype ersity within populations, and it selects both for sex-independent segregation of mitochondrion-interacting genes and for paternal leakage. These effects of genetic linkage evolution can eliminate male-harming fitness effects of mtDNA mutational ersity. With maternal mitochondrial inheritance, females maintain a tight mitochondrial-nuclear match, but males accumulate mismatch mutations because of the weak statistical associations between the two genomic components. Sex-independent segregation of mitochondria-interacting loci improves the mito-nuclear match. In a sexually antagonistic evolutionary process, male nuclear alleles evolve to increase the rate of recombination, while females evolve to suppress it. Paternal leakage of mitochondria can evolve as an alternative mechanism to improve the mito-nuclear linkage. Our modelling framework provides an evolutionary explanation for the observed paucity of mitochondrion-interacting genes on mammalian sex chromosomes and for paternal leakage in protists, plants, fungi, and some animals.
Publisher: Springer Science and Business Media LLC
Date: 27-01-2022
Publisher: Wiley
Date: 05-2021
DOI: 10.1111/JEB.13776
Abstract: Across eukaryotes, genes encoding bioenergetic machinery are located in both mitochondrial and nuclear DNA, and incompatibilities between the two genomes can be devastating. Mitochondria are often inherited maternally, and theory predicts sex‐specific fitness effects of mitochondrial mutational ersity. Yet how evolution acts on linkage patterns between mitochondrial and nuclear genomes is poorly understood. Using novel mito‐nuclear population‐genetic models, we show that the interplay between nuclear and mitochondrial genes maintains mitochondrial haplotype ersity within populations, and selects both for sex‐independent segregation of mitochondrion‐interacting genes and for paternal leakage. These effects of genetic linkage evolution can eliminate male‐harming fitness effects of mtDNA mutational ersity. With maternal mitochondrial inheritance, females maintain a tight mitochondrial–nuclear match, but males accumulate mismatch mutations because of the weak statistical associations between the two genomic components. Sex‐independent segregation of mitochondria‐interacting loci improves the mito‐nuclear match. In a sexually antagonistic evolutionary process, male nuclear alleles evolve to increase the rate of recombination, whereas females evolve to suppress it. Paternal leakage of mitochondria can evolve as an alternative mechanism to improve the mito‐nuclear linkage. Our modelling framework provides an evolutionary explanation for the observed paucity of mitochondrion‐interacting genes on mammalian sex chromosomes and for paternal leakage in protists, plants, fungi and some animals.
Publisher: The Royal Society
Date: 08-12-2021
Abstract: Uniparental inheritance (UPI) of mitochondria predominates over biparental inheritance (BPI) in most eukaryotes. However, ex les of BPI of mitochondria, or paternal leakage, are becoming increasingly prevalent. Most reported cases of BPI occur in hybrids of distantly related sub-populations. It is thought that BPI in these cases is maladaptive caused by a failure of female or zygotic autophagy machinery to recognize ergent male-mitochondrial DNA ‘tags’. Yet recent theory has put forward ex les in which BPI can evolve under adaptive selection, and empirical studies across numerous metazoan taxa have demonstrated outbreeding depression in hybrids attributable to disruption of population-specific mitochondrial and nuclear genotypes (mitonuclear mismatch). Based on these developments, we hypothesize that BPI may be favoured by selection in hybridizing populations when fitness is shaped by mitonuclear interactions. We test this idea using a deterministic, simulation-based population genetic model and demonstrate that BPI is favoured over strict UPI under moderate levels of gene flow typical of hybridizing populations. Our model suggests that BPI may be stable, rather than a transient phenomenon, in hybridizing populations.
Location: United Kingdom of Great Britain and Northern Ireland
No related grants have been discovered for Arunas Radzvilavicius.