ArticleNature communications2018
Mice lacking the mitochondrial exonuclease MGME1 accumulate mtDNA deletions without developing progeria.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 1 of them a synthesis that pooled it.
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Who cites it
53 citing papers in PubMed, 1 synthesis or guideline pooled it, 73 citations in OpenAlex.
- Non-coding RNAs and Mitochondrial Dysfunction in Alzheimer's Disease: A Systematic Review.Molecular neurobiology · 2026Pooled it
- Mitochondrial quality control in health and disease: mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2026Review
- Persistence of large mtDNA rearrangements linked to premature aging in Pol γ exonuclease-deficient mice.Nucleic acids research · 2026Article
- Single-cell multi-omic analysis of mitochondrial mutational mosaicism and dynamics.Nature communications · 2026Article
- POLRMT overexpression increases mtDNA transcription without affecting steady-state mRNA levels.Life science alliance · 2025Article
- Article
- Mitochondrial exonuclease EXOG supports DNA integrity by the removal of single-stranded DNA flaps.Nucleic acids research · 2025Article
- Nuclease-induced stepwise photodropping (NISP) to precisely investigate single-stranded DNA degradation behaviors of exonucleases and endonucleases.Nucleic acids research · 2024Article
- Novel mitochondrial-related gene signature predicts prognosis and immunological status in glioma.Translational cancer research · 2024Article
- UV damage induces production of mitochondrial DNA fragments with specific length profiles.Genetics · 2024Article
- Mechanisms and pathologies of human mitochondrial DNA replication and deletion formation.The Biochemical journal · 2024Review
- Structural basis of how MGME1 processes DNA 5' ends to maintain mitochondrial genome integrity.Nucleic acids research · 2024Article
- Decoding the mitochondria without a code: mechanistic insights into mitochondrial DNA depletion syndromes.Journal of biosciences · 2024Review
- UV damage induces production of mitochondrial DNA fragments with specific length profiles.bioRxiv : the preprint server for biology · 2023Article
- Structure-specific roles for PolG2-DNA complexes in maintenance and replication of mitochondrial DNA.Nucleic acids research · 2023Article
- Maintenance of Flap Endonucleases for Long-Patch Base Excision DNA Repair in Mouse Muscle and Neuronal Cells Differentiated In Vitro.International journal of molecular sciences · 2023Article
- Key Amino Acid Residues of Mitochondrial Transcription Factor A Synergize with Abasic (AP) Site Dynamics To Facilitate AP-Lyase Reactions.ACS chemical biology · 2023Article
- MGME1 associates with poor prognosis and is vital for cell proliferation in lower-grade glioma.Aging · 2023Article
- DNA-protein cross-links between abasic DNA damage and mitochondrial transcription factor A (TFAM).Nucleic acids research · 2023Article
- Studying Mitochondrial Nucleic Acid Synthesis Utilizing Intact Isolated Mitochondria.Methods in molecular biology (Clifton, N.J.) · 2023Article
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Replication of mammalian mitochondrial DNA (mtDNA) is an essential process that requires high fidelity and control at multiple levels to ensure proper mitochondrial function. Mutations in the mitochondrial genome maintenance exonuclease 1 (MGME1) gene were recently reported in mitochondrial disease patients. Here, to study disease pathophysiology, we generated Mgme1 knockout mice and report that homozygous knockouts develop depletion and multiple deletions of mtDNA. The mtDNA replication stalling phenotypes vary dramatically in different tissues of Mgme1 knockout mice. Mice with MGME1 deficiency accumulate a long linear subgenomic mtDNA species, similar to the one found in mtDNA mutator mice, but do not develop progeria. This finding resolves a long-standing debate by showing that point mutations of mtDNA are the main cause of progeria in mtDNA mutator mice. We also propose a role for MGME1 in the regulation of replication and transcription termination at the end of the control region of mtDNA.
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