ArticleCell death and differentiation2013
DNA damage leads to progressive replicative decline but extends the life span of long-lived mutant animals.
Article in Cell death and differentiation, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
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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.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Pharmacologic AMPK Activation Extends Lifespan inbioRxiv : the preprint server for biology · 2026Article
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- The DREAM complex functions as conserved master regulator of somatic DNA-repair capacities.Nature structural & molecular biology · 2023Article
- XPG: a multitasking genome caretaker.Cellular and molecular life sciences : CMLS · 2022Review
- Review
- Analysis of representative mutants for key DNA repair pathways on healthspan in Caenorhabditis elegans.Mechanisms of ageing and development · 2021Article
- C. elegans TFIIH subunit GTF-2H5/TTDA is a non-essential transcription factor indispensable for DNA repair.Communications biology · 2021Article
- Article
- DNA topoisomerase 3 is required for efficient germ cell quality control.The Journal of cell biology · 2021Article
- Cockayne syndrome proteins CSA and CSB maintain mitochondrial homeostasis through NADAging cell · 2020Article
- A C. elegans model for neurodegeneration in Cockayne syndrome.Nucleic acids research · 2020Article
- Identifying longevity associated genes by integrating gene expression and curated annotations.PLoS computational biology · 2020Article
- DNA damage responses in ageing.Open biology · 2019Review
- DNA damage and tissue repair: What we can learn from planaria.Seminars in cell & developmental biology · 2019Review
- Dysregulation of DAF-16/FOXO3A-mediated stress responses accelerates oxidative DNA damage induced aging.Redox biology · 2018Article
- Genomic Approach to Understand the Association of DNA Repair with Longevity and Healthy Aging Using Genomic Databases of Oldest-Old Population.Oxidative medicine and cellular longevity · 2018Review
- Systematic analysis of DNA crosslink repair pathways during development and aging in Caenorhabditis elegans.Nucleic acids research · 2017Article
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- Review
- Observational
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 4 countries.
Funding
Abstract
Human-nucleotide-excision repair (NER) deficiency leads to different developmental and segmental progeroid symptoms of which the pathogenesis is only partially understood. To understand the biological impact of accumulating spontaneous DNA damage, we studied the phenotypic consequences of DNA-repair deficiency in Caenorhabditis elegans. We find that DNA damage accumulation does not decrease the adult life span of post-mitotic tissue. Surprisingly, loss of functional ERCC-1/XPF even further extends the life span of long-lived daf-2 mutants, likely through an adaptive activation of stress signaling. Contrariwise, NER deficiency leads to a striking transgenerational decline in replicative capacity and viability of proliferating cells. DNA damage accumulation induces severe, stochastic impairment of development and growth, which is most pronounced in NER mutants that are also impaired in their response to ionizing radiation and inter-strand crosslinks. These results suggest that multiple DNA-repair pathways can protect against replicative decline and indicate that there might be a direct link between the severity of symptoms and the level of DNA-repair deficiency in patients.
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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.