ArticleCommunications biology2021
FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- FANCI promotes esophageal squamous cell carcinoma progression and cell cycle regulation and interacts with FANCD2.Journal of gastrointestinal oncology · 2026Article
- Evolutionarily Conserved but Mechanistically Distinct Mitochondrial Responses to Loss of Timeless/Swi1.Biomolecules · 2026Article
- Fanconi Anemia: Interplay Between DNA Repair Defects, Mitochondrial Dysfunction, and Oxidative Stress.Cells · 2026Review
- Radiation-induced autophagy regulates fibroblast mitochondrial metabolism and crosstalk with triple-negative breast cancer cells.Cell reports · 2026Article
- The tight bond between Fanconi anemia and aging.Frontiers in aging · 2026Review
- UBL5 and Its Role in Viral Infections.Viruses · 2024Review
- FANCD2 genome binding is nonrandom and is enriched at large transcriptionally active neural genes prone to copy number variation.Functional & integrative genomics · 2024Article
- Altered Mitochondrial Dynamic in Lymphoblasts and Fibroblasts Mutated forInternational journal of molecular sciences · 2023Article
- Replication stress increases mitochondrial metabolism and mitophagy in FANCD2 deficient fetal liver hematopoietic stem cells.Frontiers in oncology · 2023Article
- FANCD2 promotes mitotic rescue from transcription-mediated replication stress in SETX-deficient cancer cells.Communications biology · 2022Article
- Article
- Review
- Beyond base excision repair: an evolving picture of mitochondrial DNA repair.Bioscience reports · 2021Review
- UBL5/Hub1: An Atypical Ubiquitin-Like Protein with a Typical Role as a Stress-Responsive Regulator.International journal of molecular sciences · 2021Review
- Transcriptomic Changes Following Partial Depletion of CENP-E in Normal Human Fibroblasts.Genes · 2021Article
- Locus-specific transcription silencing at the FHIT gene suppresses replication stress-induced copy number variant formation and associated replication delay.Nucleic acids research · 2021Article
- Mitochondrial Control of Genomic Instability in Cancer.Cancers · 2021Review
- Beyond DNA repair and chromosome instability-Fanconi anaemia as a cellular senescence-associated syndrome.Cell death and differentiation · 2021Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and promotes CFS gene stability. Mechanistically, we demonstrate that the mitochondrial stress-dependent induction of CFS genes is mediated by ubiquitin-like protein 5 (UBL5), and that a UBL5-FANCD2 dependent axis regulates the mitochondrial UPR in human cells. We propose that FANCD2 coordinates nuclear and mitochondrial activities to prevent genome instability.
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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.