DNA repair mechanisms in dividing and non-dividing cells
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DNA damage created by endogenous or exogenous genotoxic agents can exist in multiple forms, and if allowed to persist, can promote genome instability and directly lead to various human diseases, particularly cancer, neurological abnormalities, immunodeficiency and premature aging. To avoid such deleterious outcomes, cells have evolved an array of DNA repair pathways, which carry out what is typically a multiple-step process to resolve specific DNA lesions and maintain genome integrity. To fully appreciate the biological contributions of the different DNA repair systems, one must keep in mind the cellular context within which they operate. For example, the human body is composed of non-dividing and dividing cell types, including, in the brain, neurons and glial cells. We describe herein the molecular mechanisms of the different DNA repair pathways, and review their roles in non-dividing and dividing cells, with an eye toward how these pathways may regulate the development of neurological disease.
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Although some homology-directed repair has been observed in non-dividing cells such as neurons, other DNA repair pathways than homologous recombination are more active in these long-lived postmitotic cells.
“Although a certain level of homology-directed repair has been observed in non-dividing cells, such as neurons [52], other DNA repair pathways than homologous recombination are more active in these long-lived postmitotic cells [53].”
From Circumventing the packaging limit of AAV-mediated gene replacement therapy for neurological disorders (2022) · cites this paper as [53]
CSB can interact with several members of the BER pathway, including PARP1, NEIL1 DNA glycosylase, and APE1.
“For CSB, it is already known that it can interact with several members of BER pathway, including the strandbreak response protein poly(ADP-ribose) polymerase-1 (PARP1), endonuclease VIII-like 1 (NEIL1) DNA glycosylase, and APE1 [227].”
From Sunlight damage to cellular DNA: focus on oxidatively generated lesions (2017) · cites this paper as [227]
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Connecting the Dots: From DNA Damage and Repair to Aging
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- Authors
- Iyama, T., & Wilson, D. M.
- Affiliations
- National Institutes of Health (US)
- Corresponding author
- Wilson, David M.
- ORCID
- Wilson, David M.
- Venue
- DNA Repair
- Publisher
- Elsevier BV
- Published
- 2013-08
- Volume
- 12
- Issue
- 8
- Pages
- 620-636
- ISSN
- 1568-7856 (ISSN-L)
- 1568-7864
- PMC
- PMC3720834
- OpenAlex
- W2004257622
- Cited by
- 697
- References
- 280
- Citations by year
- 2026: 20 · 2025: 37 · 2024: 49 · 2023: 56 · 2022: 43 · 2021: 69 · 2020: 58 · 2019: 59 · 2018: 65 · 2017: 57 · 2016: 72 · 2015: 62 · 2014: 47 · 2013: 2
- FWCI
- 27.17
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- DNA repair (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- National Institutes of Health
- National Institute on Aging (ZIAAG000751)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Keywords
- DNA repair pathways, genome stability, genetic damage, dividing cells, non-dividing cells, neurons, glial cells, neurological disorders, cancer, premature aging, immunodeficiency, DNA lesions
- MeSH terms
- Animals, Disease Models, Animal, DNA, DNA Damage, DNA Repair, Humans, Neurons, Pyrimidine Dimers, O(6)-Methylguanine-DNA Methyltransferase
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