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Translesion DNA Polymerases
Open accessAbstract
Living cells are continually exposed to DNA-damaging agents that threaten their genomic integrity. Although DNA repair processes rapidly target the damaged DNA for repair, some lesions nevertheless persist and block genome duplication by the cell's replicase. To avoid the deleterious consequence of a stalled replication fork, cells use specialized polymerases to traverse the damage. This process, termed "translesion DNA synthesis" (TLS), affords the cell additional time to repair the damage before the replicase returns to complete genome duplication. In many cases, this damage-tolerance mechanism is error-prone, and cell survival is often associated with an increased risk of mutagenesis and carcinogenesis. Despite being tightly regulated by a variety of transcriptional and posttranslational controls, the low-fidelity TLS polymerases also gain access to undamaged DNA where their inaccurate synthesis may actually be beneficial for genetic diversity and evolutionary fitness.
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“Pol η and Pol ζ can bypass T-T CPDs and were shown to play an important role in TLS of UV damage, while REV1 was shown to be required for bypass of a 6-4 TT dimer in vivo.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [125]
In the citing paper
“Damage tolerance is certainly an unusual repair mechanism employed in response to UV radiation. It allows rapid prevention of consequences of the replication fork arrest [125].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [125]
In the citing paper
“Furthermore, it prevents the formation of double strand breaks in response to UV radiation [125,127].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [125]
In the citing paper
“Moreover, TLS polymerases lack the 3′-5′ exonucleases (proofreading) activity further limiting repair accuracy [125,127].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [125]
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DNA replication: Mechanisms and therapeutic interventions for diseases
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Metadata
- Authors
- Goodman, M. F., & Woodgate, R.
- Affiliations
- University of Southern California (US)
- National Institutes of Health (US)
- ORCID
- Woodgate, R.
- Venue
- Cold Spring Harbor Perspectives in Biology
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2013-07-09
- Volume
- 5
- Issue
- 10
- Pages
- a010363-a010363
- ISSN
- 1943-0264 (ISSN-L)
- PMC
- PMC3783050
- OpenAlex
- W1971658781
- Cited by
- 317
- References
- 163
- Citations by year
- 2026: 35 · 2025: 19 · 2024: 14 · 2023: 16 · 2022: 30 · 2021: 26 · 2020: 31 · 2019: 22 · 2018: 25 · 2017: 32 · 2016: 22 · 2015: 28 · 2014: 11 · 2013: 6
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Cold Spring Harbor Perspectives in Biology (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (GM21422, ES012259)
- National Institute of General Medical Sciences (GM 21422, R37GM021422, R01GM021422)
- National Institute of Environmental Health Sciences (ES012259, R01ES012259)
- National Institute of Child Health and Human Development
- Eunice Kennedy Shriver National Institute of Child Health and Human Development
- 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
- Health Sciences › Medicine › Pathology and Forensic Medicine › Genetic factors in colorectal cancer
- Keywords
- translesion synthesis, DNA polymerase, DNA damage tolerance, replication fork stalling, whole-genome duplication, mutagenesis, carcinogenesis, post-translational regulation, transcriptional regulation, DNA repair, genetic diversity
- MeSH terms
- Archaea, DNA Damage, DNA-Directed DNA Polymerase, DNA Repair, DNA Replication, Escherichia coli, Humans, Models, Genetic, Saccharomyces cerevisiae, Mutagenesis
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