ArticleMechanisms of ageing and development
Deletion of Ku80 causes early aging independent of chronic inflammation and Rag-1-induced DSBs.
Article in Mechanisms of ageing and development. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 23 citations in OpenAlex.
- RAD51 separation of function mutation disables replication fork maintenance but preserves DSB repair.iScience · 2024Article
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- Doxycycline Attenuated Ethanol-Induced Inflammaging in Endothelial Cells: Implications in Alcohol-Mediated Vascular Diseases.Antioxidants (Basel, Switzerland) · 2022Article
- The multifaceted roles of DNA repair and replication proteins in aging and obesity.DNA repair · 2021Review
- Connecting the Dots: From DNA Damage and Repair to Aging.International journal of molecular sciences · 2016Review
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- Article
- Ku70 and non-homologous end joining protect testicular cells from DNA damage.Journal of cell science · 2013Article
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- Cellular senescence and organismal ageing in the absence of p21(CIP1/WAF1) in ku80(-/-) mice.EMBO reports · 2009Article
- Ku80 deletion suppresses spontaneous tumors and induces a p53-mediated DNA damage response.Cancer research · 2008Article
- DNA double-strand breaks: a potential causative factor for mammalian aging?Mechanisms of ageing and developmentReview
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Animal models of premature aging are often defective for DNA repair. Ku80-mutant mice are disabled for nonhomologous end joining; a pathway that repairs both spontaneous DNA double-strand breaks (DSBs) and induced DNA DSBs generated by the action of a complex composed of Rag-1 and Rag-2 (Rag). Rag is essential for inducing DSBs important for assembling V(D)J segments of antigen receptor genes that are required for lymphocyte development. Thus, deletion of either Rag-1 or Ku80 causes severe combined immunodeficiency (scid) leading to chronic inflammation. In addition, Rag-1 induces breaks at non-B DNA structures. Previously we reported Ku80-mutant mice undergo premature aging, yet we do not know the root cause of this phenotype. Early aging may be caused by either defective repair of spontaneous DNA damage, defective repair of Rag-1-induced breaks or chronic inflammation caused by scid. To address this issue, we analyzed aging in control and Ku80-mutant mice deleted for Rag-1 such that both cohorts are scid and suffer from chronic inflammation. We make two observations: (1) chronic inflammation does not cause premature aging in these mice and (2) Ku80-mutant mice exhibit early aging independent of Rag-1. Therefore, this study supports defective repair of spontaneous DNA damage as the root cause of early aging in Ku80-mutant mice.
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