ArticleScience (New York, N.Y.)2016
Mitochondrial endonuclease G mediates breakdown of paternal mitochondria upon fertilization.
Article in Science (New York, N.Y.), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 101 papers, 2 of them syntheses that pooled it.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
101 citing papers in PubMed, 2 syntheses or guidelines pooled it, 199 citations in OpenAlex.
- Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)Autophagy · 2021Guideline
- Selective autophagy of intracellular organelles: recent research advances.Theranostics · 2021Pooled it
- Regulation of mitochondrial function during spermatogenesis and sperm maturation.Cellular & molecular biology letters · 2026Review
- Human Endonuclease G Preferentially Cleaves Oxidatively Damaged DNA.Biochemistry · 2026Article
- Mitochondria and the epigenome: maternal co-inheritance and crosstalk from oocyte to embryo.Cell communication and signaling : CCS · 2026Review
- ATG5-HSP90.2-mediated micromitophagy as a cytological basis for maternal inheritance of plant mitochondria.Nature plants · 2026Article
- ALKB-1-dependent tRNA methylation is required for efficient paternal mitochondrial elimination.Nature communications · 2026Article
- Gatekeepers of the Germ Line: How Mitochondria Shape Reproductive Evolution in Metazoans.Biology · 2025Review
- Induction of postmeiotic DNA double-strand breaks by the Pnu1 endonuclease inMolecular biology of the cell · 2025Article
- Phosphomimetic Experiments Do Not Support a Causal Role for TFAM Phosphorylation in mtDNA Elimination in Sperm.Journal of molecular biology · 2025Article
- Article
- Mitochondrial curation for the next generation.Current opinion in genetics & development · 2025Review
- Asymmetric partitioning of persistent paternal mitochondria during cell divisions safeguards embryo development and mitochondrial inheritance.Developmental cell · 2025Article
- A nuclear-encoded endonuclease governs the paternal transmission of mitochondria in Cucumis plants.Nature communications · 2025Article
- Reply to: An alternative model for maternal mtDNA inheritance.Nature genetics · 2025Article
- Review
- Review
- Endonuclease G promotes hepatic mitochondrial respiration by selectively increasing mitochondrial tRNAProceedings of the National Academy of Sciences of the United States of America · 2025Article
- Modes and mechanisms for the inheritance of mitochondria and plastids in pathogenic protists.PLoS pathogens · 2025Review
- Probing the importance of AIF interaction with endonuclease G in mitochondrial inheritance and neurodegeneration.Cell discovery · 2024Article
41 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Mitochondria are inherited maternally in most animals, but the mechanisms of selective paternal mitochondrial elimination (PME) are unknown. While examining fertilization in Caenorhabditis elegans, we observed that paternal mitochondria rapidly lose their inner membrane integrity. CPS-6, a mitochondrial endonuclease G, serves as a paternal mitochondrial factor that is critical for PME. We found that CPS-6 relocates from the intermembrane space of paternal mitochondria to the matrix after fertilization to degrade mitochondrial DNA. It acts with maternal autophagy and proteasome machineries to promote PME. Loss of cps-6 delays breakdown of mitochondrial inner membranes, autophagosome enclosure of paternal mitochondria, and PME. Delayed removal of paternal mitochondria causes increased embryonic lethality, demonstrating that PME is important for normal animal development. Thus, CPS-6 functions as a paternal mitochondrial degradation factor during animal development.
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Registered trials
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.