ArticleHeredity2024
Dissecting the sequential evolution of a selfish mitochondrial genome in Caenorhabditis elegans.
Article in Heredity, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Mutational biases and selection in mitochondrial genomes: insights from a comparative analysis of natural and laboratory populations of Caenorhabditis elegans.G3 (Bethesda, Md.) · 2026Article
- Effects of mating system and adaptedness on the evolution of fitness and mtDNA copy number in mitonuclear mismatched C. elegans.Heredity · 2025Article
- Selection promotes age-dependent degeneration of the mitochondrial genome.bioRxiv : the preprint server for biology · 2024Article
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Authors and funding
3 authors.
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Abstract
Mitochondrial genomes exist in a nested hierarchy of populations where mitochondrial variants are subject to genetic drift and selection at each level of organization, sometimes engendering conflict between different levels of selection, and between the nuclear and mitochondrial genomes. Deletion mutants in the Caenorhabditis elegans mitochondrial genome can reach high intracellular frequencies despite strongly detrimental effects on fitness. During a mutation accumulation (MA) experiment in C. elegans, a 499 bp deletion in ctb-1 rose to 90% frequency within cells while significantly reducing fitness. During the experiment, the deletion-bearing mtDNA acquired three additional mutations in nd5, namely two single insertion frameshift mutations in a homopolymeric run, and a base substitution. Despite an additional fitness cost of these secondary mutations, all deletion-bearing molecules contained the nd5 mutations at the termination of the MA experiment. The presence of mutant mtDNA was associated with increased mtDNA copy-number. Variation in mtDNA copy-number was greater in the MA lines than in a wildtype nuclear background, including a severe reduction in copy-number at one generational timepoint. Evolutionary replay experiments using different generations of the MA experiment as starting points suggests that two of the secondary mutations contribute to the proliferation of the original ctb-1 deletion by unknown mechanisms.
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