Incorporation of a nucleoside analog maps genome repair sites in postmitotic human neurons
Open accessAbstract
Neurons are the longest-lived cells in our bodies and lack DNA replication, which makes them reliant on a limited repertoire of DNA repair mechanisms to maintain genome fidelity. These repair mechanisms decline with age, but we have limited knowledge of how genome instability emerges and what strategies neurons and other long-lived cells may have evolved to protect their genomes over the human life span. A targeted sequencing approach in human embryonic stem cell-induced neurons shows that, in neurons, DNA repair is enriched at well-defined hotspots that protect essential genes. These hotspots are enriched with histone H2A isoforms and RNA binding proteins and are associated with evolutionarily conserved elements of the human genome. These findings provide a basis for understanding genome integrity as it relates to aging and disease in the nervous system.
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The process of BER erasing oxidative damaged bases and cytosine methylation could lead to base mutations.
“This process promotes extensive endogenous DNA damage in neuronal enhancers, safeguards cell identities but could also lead to base mutations12–15.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [13]
The paper’s discussion of DNA repair hotspots (section labeled Abstract; page unavailable) says they are linked to neuronal identity and may protect essential elements from erroneous repair. It does not establish that BER removes oxidative damage or cytosine methylation in neuronal enhancers, or that this process leads to base mutations; its comparison found no enrichment of single-nucleotide variants near repair hotspots. (LLM, conf=0.78)
Experimental — accuracy not yet measuredThe process of BER erasing oxidative damaged bases and cytosine methylation promotes extensive endogenous DNA damage in neuronal enhancers.
“This process promotes extensive endogenous DNA damage in neuronal enhancers, safeguards cell identities but could also lead to base mutations12–15.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [13]
The paper’s Repair-seq findings (Fig. 1D and Fig. 2A) identify numerous DNA-repair hotspots in induced human neurons, some in open chromatin and active regulatory regions. It does not establish that base-excision repair of oxidative damage or cytosine methylation causes extensive damage specifically in neuronal enhancers; its discussion of mutations reports no enrichment near the hotspots (Fig. 4A). (LLM, conf=0.85)
Experimental — accuracy not yet measuredThe process of BER erasing oxidative damaged bases and cytosine methylation safeguards cell identities.
“This process promotes extensive endogenous DNA damage in neuronal enhancers, safeguards cell identities but could also lead to base mutations12–15.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [13]
In the indexed paper’s Abstract-labeled text (no page given), DNA repair hotspots are associated with genes essential for neuronal identity, and the authors suggest that the hotspots might protect essential elements from erroneous or absent repair. The copy does not identify this process as BER erasing oxidatively damaged bases or cytosine methylation, nor does it establish that the process promotes extensive endogenous damage in neuronal enhancers. (LLM, conf=0.84)
Experimental — accuracy not yet measuredDNA repair hotspots are enriched in a subset of regulatory regions including enhancers, to protect the identities and functions of postmitotic cells (such as neurons).
“Recent studies revealed that DNA repair hotspots are enriched in a subset of regulatory regions including enhancers, to protect the identities and functions of postmitotic cells (such as neurons)12,13,15.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [13]
The copy reports that about 23.5% of DNA repair hotspots in induced human neurons overlap open chromatin or active regulatory regions, and says the hotspots may play a role in neuronal identity and function (section labeled Abstract; page unavailable). It identifies promoter enrichment but does not establish enhancer enrichment, and it leaves open whether the findings extend to other postmitotic cells. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe observed DNA damage hotspots are combined results from DNA damage formation and repair.
“Moreover, the observed DNA damage hotspots are combined results from DNA damage formation and repair12,13.”
From Single-cell parallel analysis of DNA damage and transcriptome reveals selective genome vulnerability (2025) · cites this paper as [13]
The paper’s Abstract describes the hotspots as peaks of EdU incorporation that map DNA repair synthesis. It also reports that a DNA-damaging treatment changed which hotspots were detected, consistent with damage formation affecting the observed pattern. It does not establish that the baseline hotspots are combined results of damage formation and repair. (LLM, conf=0.78)
Experimental — accuracy not yet measured
Neurons actively induce both DSBs and single-stranded breaks as part of their normal physiology.
“neurons also actively induce both DSBs and single-stranded breaks as part of their normal physiology”
From Neuronal DNA double-strand breaks lead to genome structural variations and 3D genome disruption in neurodegeneration (2023) · cites this paper as [10]
The genomic location of DNA damage impacts neuronal activity and degeneration.
“we are just beginning to appreciate the significance of a lesion’s genomic location in relation to its effect on neuronal activity and, ultimately, degeneration”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Reid et al, 2021
DNA repair mapping reveals that postmitotic neurons accumulate breaks in regulatory elements associated with neuronal function.
“DNA repair mapping reveals that postmitotic neurons do indeed accumulate breaks in regulatory elements associated with neuronal function”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Reid et al, 2021
Genome-wide profiling of DNA breaks in post-mitotic neurons has revealed that their locations are likely major mediators of their toxicity.
“To this end, genome‐wide profiling of DNA breaks in post‐mitotic neurons have revealed that their locations are likely major mediators of their toxicity.”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Reid et al, 2021
Postmitotic neurons harbor SSBs and other forms of breaks in the regulatory regions of genes that modulate synaptic plasticity and neuronal function.
“As described earlier, the use of nucleoside analog incorporation to map DNA repair has led to the observation that postmitotic neurons harbor SSBs and other forms of breaks in the regulatory regions of genes that modulate synaptic plasticity and neuronal function (Reid et al, 2021; Wu et al, 2021).”
From Mechanisms of DNA damage-mediated neurotoxicity in neurodegenerative disease (2022) · cites this paper as Reid et al, 2021
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Caging of a Strongly Pairing Fluorescent Thymidine Analog with Soft Nucleophiles
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ZNF512B safeguards genome integrity at regulatory regions to repress the SASP and inflammation
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- Authors
- Reid, D. A., Reed, P. J., Schlachetzki, J. C. M., Nitulescu, I. I., Chou, G., Tsui, E. C., Jones, J. R., Chandran, S., Lu, A. T., McClain, C. A., Ooi, J. H., Wang, T.-W., Lana, A. J., Linker, S. B., Ricciardulli, A. S., Lau, S., Schafer, S. T., Horvath, S., Dixon, J. R., Hah, N., Glass, C. K., & Gage, F. H.
- Affiliations
- Salk Institute for Biological Studies (US)
- University of California San Diego (US)
- University of California, Los Angeles (US)
- Corresponding author
- Reid, Dylan A.
- Reed, Patrick J.
- Schlachetzki, Johannes C. M.
- Nitulescu, Ioana I.
- Chou, Grace
- Tsui, Enoch C.
- Jones, Jeffrey R.
- Gage, Fred H.
- ORCID
- Reid, Dylan A.
- Reed, Patrick J.
- Schlachetzki, Johannes C. M.
- Nitulescu, Ioana I.
- Chou, Grace
- Tsui, Enoch C.
- Jones, Jeffrey R.
- Chandran, Sahaana
- Lu, Ake T.
- McClain, Claire A.
- Ooi, Jean H.
- Wang, Tzu-Wen
- Lana, Addison J.
- Linker, Sara B.
- Ricciardulli, Anthony S.
- Lau, Shong
- Schafer, Simon T.
- Horvath, Steve
- Dixon, Jesse R.
- Hah, Nasun
- Glass, Christopher K.
- Gage, Fred H.
- Venue
- Science
- Published
- 2021-04-02
- Volume
- 372
- Issue
- 6537
- Pages
- 91-94
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- PMC
- PMC9179101
- OpenAlex
- W3151212872
- Cited by
- 121
- References
- 81
- Citations by year
- 2026: 18 · 2025: 19 · 2024: 24 · 2023: 26 · 2022: 27 · 2021: 7
- FWCI
- 6.59
- Type
- journal article
- Language
- en
- Open access
- green
- doi.org
- Licence
- cc-by-nc
- Locations
- Science (publishedVersion)
- bioRxiv (Cold Spring Harbor Laboratory) (acceptedVersion, cc-by-nc)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- eScholarship (California Digital Library) (submittedVersion)
- Funders
- NIH Office of the Director (AG056306, DP5OD023071-03)
- Alzheimer’s Association (AARF-17-504089)
- Leona M. and Harry B. Helmsley Charitable Trust
- JPB Foundation
- NIH (R01AG056411-02)
- American Heart Association/Paul G. Allen Frontiers Group Brain Health & Cognitive Impairment Initiative (19PABHI34610000)
- Dolby Charitable Trust
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA and Nucleic Acid Chemistry
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
- Keywords
- DNA repair, genomic instability, postmitotic neurons, RNA-binding proteins, embryonic stem cell-derived neurons, aging, genome stability, essential genes
- MeSH terms
- Aging, Deoxyuridine, DNA Damage, DNA Repair, Histones, Humans, Mitosis, Mutation, Nervous System Diseases, Neurons, Promoter Regions, Genetic, Transcription, Genetic, Genome, Human, RNA-Binding Proteins, Sequence Analysis, DNA, DNA, Intergenic, Genomic Instability, Embryonic Stem Cells
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