ArticleMolecular and cellular biology2018
RAD51C/XRCC3 Facilitates Mitochondrial DNA Replication and Maintains Integrity of the Mitochondrial Genome.
Article in Molecular and cellular biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 3 of them syntheses that pooled it.
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Who cites it
37 citing papers in PubMed, 3 syntheses or guidelines pooled it, 53 citations in OpenAlex.
- Association between XRCC3 p.Thr241Met polymorphism and risk of glioma: A systematic review and meta-analysis.PloS one · 2022Pooled it
- Epigenome-wide association study of mitochondrial genome copy number.Human molecular genetics · 2021Pooled it
- The association between XRCC3 rs1799794 polymorphism and cancer risk: a meta-analysis of 34 case-control studies.BMC medical genomics · 2021Pooled it
- Distinct functions of mammalian RAD51 paralogs in genome maintenance.Biochemical Society transactions · 2026Review
- MSTO1 modulates RAD51 activity to safeguard mitochondrial DNA integrity and control immune responses.Cancer gene therapy · 2026Article
- RAD51C-XRCC3 complex regulates FANCM-mediated R-loop resolution to safeguard genome integrity.Science advances · 2026Article
- Mapping the genetic landscape of suicide risk: Insights from genomic SEM.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- RNF20-mediated H2B monoubiquitination protects stalled forks from degradation and promotes fork restart.EMBO reports · 2025Article
- Disruption of mitochondrial DNA integrity in cardiomyocyte injury upon ischemia/reperfusion.Genes & diseases · 2025Review
- Complex Interplay between DNA Damage and Autophagy in Disease and Therapy.Biomolecules · 2024Review
- Evidence that Alzheimer's Disease Is a Disease of Competitive Synaptic Plasticity Gone Awry.Journal of Alzheimer's disease : JAD · 2024Review
- Comprehensive analysis of the mitochondrial genome ofFrontiers in plant science · 2024Article
- Plasma proteomics show altered inflammatory and mitochondrial proteins in patients with neurologic symptoms of post-acute sequelae of SARS-CoV-2 infection.Brain, behavior, and immunity · 2023Article
- Uncharacterized protein C17orf80 - a novel interactor of human mitochondrial nucleoids.Journal of cell science · 2023Article
- Origin of minicircular mitochondrial genomes in red algae.Nature communications · 2023Article
- REC drives recombination to repair double-strand breaks in animal mtDNA.The Journal of cell biology · 2023Article
- Direct evidence of CRISPR-Cas9-mediated mitochondrial genome editing.Innovation (Cambridge (Mass.)) · 2022Article
- Parkinson's Disease Phenotypes in Patient Neuronal Cultures and Brain Organoids Improved by 2-Hydroxypropyl-β-Cyclodextrin Treatment.Movement disorders : official journal of the Movement Disorder Society · 2022Article
- Recent Advances in the Development of Non-PIKKs Targeting Small Molecule Inhibitors of DNA Double-Strand Break Repair.Frontiers in oncology · 2022Review
- Liensinine Inhibits Cell Growth and Blocks Autophagic Flux in Nonsmall-Cell Lung Cancer.Journal of oncology · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mechanisms underlying mitochondrial genome maintenance have recently gained wide attention, as mutations in mitochondrial DNA (mtDNA) lead to inherited muscular and neurological diseases, which are linked to aging and cancer. It was previously reported that human RAD51, RAD51C, and XRCC3 localize to mitochondria upon oxidative stress and are required for the maintenance of mtDNA stability. Since RAD51 and RAD51 paralogs are spontaneously imported into mitochondria, their precise role in mtDNA maintenance under unperturbed conditions remains elusive. Here, we show that RAD51C/XRCC3 is an additional component of the mitochondrial nucleoid having nucleus-independent roles in mtDNA maintenance. RAD51C/XRCC3 localizes to the mtDNA regulatory regions in the D-loop along with the mitochondrial polymerase POLG, and this recruitment is dependent upon Twinkle helicase. Moreover, upon replication stress, RAD51C and XRCC3 are further enriched at the mtDNA mutation hot spot region D310. Notably, the absence of RAD51C/XRCC3 affects the stability of POLG on mtDNA. As a consequence, RAD51C/XRCC3-deficient cells exhibit reduced mtDNA synthesis and increased lesions in the mitochondrial genome, leading to overall unhealthy mitochondria. Together, these findings lead to the proposal of a mechanism for a direct role of RAD51C/XRCC3 in maintaining mtDNA integrity under replication stress conditions.
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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.