ArticleBMC genetics2007
A persistent mitochondrial deletion reduces fitness and sperm performance in heteroplasmic populations of C. elegans.
Article in BMC genetics, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 81 citations in OpenAlex.
- Mutational biases and selection in mitochondrial genomes: insights from a comparative analysis of natural and laboratory populations of Caenorhabditis elegans.G3 (Bethesda, Md.) · 2026Article
- Programmed mitophagy at the oocyte-to-zygote transition promotes lineage endurance.Nature cell biology · 2026Article
- Multiple distinct evolutionary mechanisms govern the dynamics of selfish mitochondrial genomes in Caenorhabditis elegans.Nature communications · 2024Article
- Dissecting the sequential evolution of a selfish mitochondrial genome in Caenorhabditis elegans.Heredity · 2024Article
- Friend turned foe: selfish behavior of a spontaneously arising mitochondrial deletion in an experimentally evolved Caenorhabditis elegans population.G3 (Bethesda, Md.) · 2024Article
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- Identification of candidate mitochondrial inheritance determinants using the mammalian cell-free system.eLife · 2023Article
- Article
- Mitochondrial dysfunction, aging, and the mitochondrial unfolded protein response in Caenorhabditis elegans.Genetics · 2022Review
- Mutant C. elegans mitofusin leads to selective removal of mtDNA heteroplasmic deletions across generations to maintain fitness.BMC biology · 2022Article
- Natural and Artificial Mechanisms of Mitochondrial Genome Elimination.Life (Basel, Switzerland) · 2021Review
- Nutrient status shapes selfish mitochondrial genome dynamics across different levels of selection.eLife · 2020Article
- Loss of flavin adenine dinucleotide (FAD) impairs sperm function and male reproductive advantage ineLife · 2020Article
- The conflict within: origin, proliferation and persistence of a spontaneously arising selfish mitochondrial genome.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2020Article
- Complex Transmission Patterns and Age-Related Dynamics of a Selfish mtDNA Deletion.Integrative and comparative biology · 2019Article
- Emerging topics in C. elegans aging research: Transcriptional regulation, stress response and epigenetics.Mechanisms of ageing and development · 2019Review
- Clonal expansion of mitochondrial DNA deletions is a private mechanism of aging in long-lived animals.Aging cell · 2018Article
- Hydrogen peroxide produced by superoxide dismutase SOD-2 activates sperm inThe Journal of biological chemistry · 2017Article
- Chemosensory and hyperoxia circuits in C. elegans males influence sperm navigational capacity.PLoS biology · 2017Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundMitochondrial DNA (mtDNA) mutations are of increasing interest due to their involvement in aging, disease, fertility, and their role in the evolution of the mitochondrial genome. The presence of reactive oxygen species and the near lack of repair mechanisms cause mtDNA to mutate at a faster rate than nuclear DNA, and mtDNA deletions are not uncommon in the tissues of individuals, although germ-line mtDNA is largely lesion-free. Large-scale deletions in mtDNA may disrupt multiple genes, and curiously, some large-scale deletions persist over many generations in a heteroplasmic state. Here we examine the phenotypic effects of one such deletion, uaDf5, in Caenorhabditis elegans (C. elegans). Our study investigates the phenotypic effects of this 3 kbp deletion.
resultsThe proportion of uaDf5 chromosomes in worms was highly heritable, although uaDf5 content varied from worm to worm and within tissues of individual worms. We also found an impact of the uaDf5 deletion on metabolism. The deletion significantly reduced egg laying rate, defecation rate, and lifespan. Examination of sperm bearing the uaDf5 deletion revealed that sperm crawled more slowly, both in vitro and in vivo.
conclusionWorms harboring uaDf5 are at a selective disadvantage compared to worms with wild-type mtDNA. These effects should lead to the rapid extinction of the deleted chromosome, but it persists indefinitely. We discuss both the implications of this phenomenon and the possible causes of a shortened lifespan for uaDf5 mutant worms.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.