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Pyrimidine Dimers

Genetics and Genomics · NLM MeSH · updated 2026-10-29 · version 1

Citations verified against PubMedNot yet clinician-reviewed10 referencesApproximately 4 min read

Dimers found in DNA chains damaged by ultraviolet rays.

Table of Contents

1. Definition2. Research landscape3. Reading the evidence4. Open-access studies5. Key reviews6. References7. About this article

Definition and research guide

This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.

Content available: 4 complete abstracts (750 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.

Definition

Dimers found in DNA chains damaged by ultraviolet rays. They consist of two adjacent pyrimidine nucleotides, usually thymine nucleotides, in which the pyrimidine residues are covalently joined by a cyclobutane ring. These dimers block dna replication.

Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.

Also known as: Cyclobutane Pyrimidine Dimer; Cyclobutane Pyrimidine Dimers; Pyrimidine Dimer, Cyclobutane; Pyrimidine Dimers, Cyclobutane; Cyclobutane-Pyrimidine Dimers; Pyrimidine Dimer; Cyclobutane-Pyrimidine Dimer; Cytosine-Thymine Dimers.

Where it fits in the MeSH classification

Broader topics
Pyrimidine Nucleotides; Oligonucleotides; DNA Damage
See also
DNA Damage

Related concepts

  • Ultraviolet Rays
  • Pyrimidine Nucleotides
  • Thymine
  • Dna Replication

Research landscape

PubMed indexes 2,680 records tagged with the MeSH heading “Pyrimidine Dimers” (counts retrieved 2026-10-29). 262 of them (9.8%) were published from 2020 onward, and the busiest period so far is through 1999 with 1,267 records.

Reviews account for 190 records (7.1%) and meta-analyses for 0. Randomized controlled trials number 7 (0.3%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.

PubMed records by publication periodthrough 1999: 1,267 records; 2000-2009: 641 records; 2010-2019: 510 records; 2020 onward: 262 records1,267through 19996412000-20095102010-20192622020 onward
Records in PubMed indexed with this heading, by publication period. Real counts from NCBI E-utilities; the final period covers only part of the current year. Volume reflects how much has been published, not how strong the evidence is.
Show the data
PeriodRecords
through 19991,267
2000-2009641
2010-2019510
2020 onward262
Share of records by publication typeReviews: 7.1 percent; Meta-analyses: 0.0 percent; Randomized controlled trials: 0.3 percentReviews7.1% (190)Meta-analyses0.0% (0)Randomized controlled trials0.3% (7)
Share of all PubMed records on this heading that carry each publication type. Types overlap with other records, so the shares do not sum to 100%.
Publication-type chart data
Publication types among 2,680 PubMed records
TypeRecordsShare
Reviews1907.1%
Meta-analyses00.0%
Randomized controlled trials70.3%

Method: PubMed query "Pyrimidine Dimers"[MeSH Terms] with publication-type and date filters, retrieved 2026-10-29.

Reading the evidence in genetics and genomics

Genetic findings vary widely in strength. A variant linked to a condition in one study may not replicate in other ancestries, and most common variants have small effects that are meaningful only in aggregate. Studies of rare, high-impact variants can support strong causal claims about a gene, while association studies describe statistical links that need functional and independent replication. Check the sample size, the ancestry of participants, whether results were replicated, and whether a laboratory or clinical outcome was actually measured.

Evidence from open-access studies

These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.

Study comparison — selected abstracts, not a systematic review
Study / authorsYearSource label / designEurope PMC citationsLicence / source
High resolution mapping of modified DNA nucleobases using excision repair enzymes
Bryan DS, Ransom M, Adane B, York K, Hesselberth JR
2014Research article
Design not recorded in structured metadata
72cc by
PMID 25015380 · DOI · PMC4158761
Analysis of DNA repair and protection in the Tardigrade Ramazzottius varieornatus and Hypsibius dujardini after exposure to UVC radiation
Horikawa DD, Cumbers J, Sakakibara I, Rogoff D, Leuko S, Harnoto R, et al.
2013Research article
Design not recorded in structured metadata
70cc0
PMID 23762256 · DOI · PMC3675078
Single-molecule visualization reveals the damage search mechanism for the human NER protein XPC-RAD23B
Cheon NY, Kim HS, Yeo JE, Schärer OD, Lee JY
2019Research article
Design not recorded in structured metadata
64cc by
PMID 31372632 · DOI · PMC6895271
Conservation of dark CPD photolyase function in blind cavefish
Li H, Scheitle C, Di Mauro G, Fuselli S, Fritsch-Decker S, Todo T, et al.
2025Research article
Design not recorded in structured metadata
5cc by
PMID 40790130 · DOI · PMC12340131

High resolution mapping of modified DNA nucleobases using excision repair enzymes [1]

Research article Bryan DS, Ransom M, Adane B, York K, Hesselberth JR · · 2014 · cited 72 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
The incorporation and creation of modified nucleobases in DNA have profound effects on genome function.
Closing excerpt
The Excision-seq method is broadly applicable for high precision, genome-wide mapping of modified nucleobases with cognate repair enzymes.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (167 words)

The incorporation and creation of modified nucleobases in DNA have profound effects on genome function. We describe methods for mapping positions and local content of modified DNA nucleobases in genomic DNA. We combined in vitro nucleobase excision with massively parallel DNA sequencing (Excision-seq) to determine the locations of modified nucleobases in genomic DNA. We applied the Excision-seq method to map uracil in E. coli and budding yeast and discovered significant variation in uracil content, wherein uracil is excluded from the earliest and latest replicating regions of the genome, possibly driven by changes in nucleotide pool composition. We also used Excision-seq to identify sites of pyrimidine dimer formation induced by UV light exposure, where the method could distinguish between sites of cyclobutane and 6-4 photoproduct formation. These UV mapping data enabled analysis of local sequence bias around pyrimidine dimers and suggested a preference for an adenosine downstream from 6-4 photoproducts. The Excision-seq method is broadly applicable for high precision, genome-wide mapping of modified nucleobases with cognate repair enzymes.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 25015380 · DOI · PMC4158761

Analysis of DNA repair and protection in the Tardigrade Ramazzottius varieornatus and Hypsibius dujardini after exposure to UVC radiation [2]

Research article Horikawa DD, Cumbers J, Sakakibara I, Rogoff D, Leuko S, Harnoto R, et al. · · 2013 · cited 70 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
Tardigrades inhabiting terrestrial environments exhibit extraordinary resistance to ionizing radiation and UV radiation although little is known about the mechanisms underlying the resistance.
Closing excerpt
Thus we propose that UV radiation tolerance in tardigrades is due to the both high capacities of DNA damage repair and DNA protection, a two-pronged survival strategy.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (224 words)

Tardigrades inhabiting terrestrial environments exhibit extraordinary resistance to ionizing radiation and UV radiation although little is known about the mechanisms underlying the resistance. We found that the terrestrial tardigrade Ramazzottius varieornatus is able to tolerate massive doses of UVC irradiation by both being protected from forming UVC-induced thymine dimers in DNA in a desiccated, anhydrobiotic state as well as repairing the dimers that do form in the hydrated animals. In R. varieornatus accumulation of thymine dimers in DNA induced by irradiation with 2.5 kJ/m(2) of UVC radiation disappeared 18 h after the exposure when the animals were exposed to fluorescent light but not in the dark. Much higher UV radiation tolerance was observed in desiccated anhydrobiotic R. varieornatus compared to hydrated specimens of this species. On the other hand, the freshwater tardigrade species Hypsibius dujardini that was used as control, showed much weaker tolerance to UVC radiation than R. varieornatus, and it did not contain a putative phrA gene sequence. The anhydrobiotes of R. varieornatus accumulated much less UVC-induced thymine dimers in DNA than hydrated one. It suggests that anhydrobiosis efficiently avoids DNA damage accumulation in R. varieornatus and confers better UV radiation tolerance on this species. Thus we propose that UV radiation tolerance in tardigrades is due to the both high capacities of DNA damage repair and DNA protection, a two-pronged survival strategy.

Abstract reproduced from the open-access article under the recorded cc0 licence; © the authors. PMID 23762256 · DOI · PMC3675078

Single-molecule visualization reveals the damage search mechanism for the human NER protein XPC-RAD23B [3]

Research article Cheon NY, Kim HS, Yeo JE, Schärer OD, Lee JY · · 2019 · cited 64 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
DNA repair is critical for maintaining genomic integrity.
Closing excerpt
Taken together, our results provide new insight into how XPC-RAD23B searches for DNA lesions in billions of base pairs in human genome.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (196 words)

DNA repair is critical for maintaining genomic integrity. Finding DNA lesions initiates the entire repair process. In human nucleotide excision repair (NER), XPC-RAD23B recognizes DNA lesions and recruits downstream factors. Although previous studies revealed the molecular features of damage identification by the yeast orthologs Rad4-Rad23, the dynamic mechanisms by which human XPC-RAD23B recognizes DNA defects have remained elusive. Here, we directly visualized the motion of XPC-RAD23B on undamaged and lesion-containing DNA using high-throughput single-molecule imaging. We observed three types of one-dimensional motion of XPC-RAD23B along DNA: diffusive, immobile and constrained. We found that consecutive AT-tracks led to increase in proteins with constrained motion. The diffusion coefficient dramatically increased according to ionic strength, suggesting that XPC-RAD23B diffuses along DNA via hopping, allowing XPC-RAD23B to bypass protein obstacles during the search for DNA damage. We also examined how XPC-RAD23B identifies cyclobutane pyrimidine dimers (CPDs) during diffusion. XPC-RAD23B makes futile attempts to bind to CPDs, consistent with low CPD recognition efficiency. Moreover, XPC-RAD23B binds CPDs in biphasic states, stable for lesion recognition and transient for lesion interrogation. Taken together, our results provide new insight into how XPC-RAD23B searches for DNA lesions in billions of base pairs in human genome.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 31372632 · DOI · PMC6895271

Conservation of dark CPD photolyase function in blind cavefish [4]

Research article Li H, Scheitle C, Di Mauro G, Fuselli S, Fritsch-Decker S, Todo T, et al. · · 2025 · cited 5 times (Europe PMC)

Abstract reading summary — source excerpts
Opening excerpt
DNA damage is generated by various environmental stressors and so DNA repair systems must inevitably adapt to changing environments.
Closing excerpt
Thereby we document selective conservation of light-independent photolyase function in blind cavefish, enabling the repair of DNA damage encountered in an extreme subterranean environment.
Interpretation limits
Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (163 words)

DNA damage is generated by various environmental stressors and so DNA repair systems must inevitably adapt to changing environments. Photolyases represent a highly conserved class of enzymes which repair UV-induced covalent crosslinks between adjacent pyrimidine bases (CPD and 6-4 photoproducts) via photoreactivation. In the blind cavefish Phreatichthys andruzzii which has evolved for millions of years completely isolated from UV radiation and visible light, we have documented multiple polymorphisms and loss of function mutations affecting both the 6-4phr and DASHphr photolyase genes while strangely, the CPDphr gene remains highly conserved. Using loss and gain of photolyase function medaka and mammalian cell lines, we reveal a novel function for CPDphr. Specifically, it enables the light-independent repair of CPD as well as 8-OHdG, an oxidatively modified form of guanosine which are both generated under oxidative stress in the absence of UV radiation. Thereby we document selective conservation of light-independent photolyase function in blind cavefish, enabling the repair of DNA damage encountered in an extreme subterranean environment.

Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40790130 · DOI · PMC12340131

Key reviews and meta-analyses

The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.

  • Research article Measuring DNA modifications with the comet assay: a compendium of protocols [5]
    Collins A, Møller P, Gajski G, Vodenková S, Abdulwahed A, Anderson D, et al. · Nat Protoc · 2023 · cited 302 times (Europe PMC)
  • Research article Photoinduced damage to cellular DNA: direct and photosensitized reactions [6]
    Cadet J, Mouret S, Ravanat JL, Douki T · Photochem Photobiol · 2012 · cited 206 times (Europe PMC)
  • Research article The mechanism of action of DNA photolyases [7]
    Carell T, Burgdorf LT, Kundu LM, Cichon M · Curr Opin Chem Biol · 2001 · cited 107 times (Europe PMC)
  • Research article Solar UV radiation-induced DNA Bipyrimidine photoproducts: formation and mechanistic insights [8]
    Cadet J, Grand A, Douki T · Top Curr Chem · 2015 · cited 95 times (Europe PMC)
  • Research article The variety of UV-induced pyrimidine dimeric photoproducts in DNA as shown by chromatographic quantification methods [9]
    Douki T · Photochem Photobiol Sci · 2013 · cited 82 times (Europe PMC)
  • Research article Photolyase: Dynamics and electron-transfer mechanisms of DNA repair [10]
    Zhang M, Wang L, Zhong D · Arch Biochem Biophys · 2017 · cited 78 times (Europe PMC)

References

  1. Bryan DS, Ransom M, Adane B, York K, Hesselberth JR. High resolution mapping of modified DNA nucleobases using excision repair enzymes. . 2014. PMID 25015380 · DOI · PMC4158761
  2. Horikawa DD, Cumbers J, Sakakibara I, Rogoff D, Leuko S, Harnoto R, et al.. Analysis of DNA repair and protection in the Tardigrade Ramazzottius varieornatus and Hypsibius dujardini after exposure to UVC radiation. . 2013. PMID 23762256 · DOI · PMC3675078
  3. Cheon NY, Kim HS, Yeo JE, Schärer OD, Lee JY. Single-molecule visualization reveals the damage search mechanism for the human NER protein XPC-RAD23B. . 2019. PMID 31372632 · DOI · PMC6895271
  4. Li H, Scheitle C, Di Mauro G, Fuselli S, Fritsch-Decker S, Todo T, et al.. Conservation of dark CPD photolyase function in blind cavefish. . 2025. PMID 40790130 · DOI · PMC12340131
  5. Collins A, Møller P, Gajski G, Vodenková S, Abdulwahed A, Anderson D, et al.. Measuring DNA modifications with the comet assay: a compendium of protocols. Nat Protoc. 2023. PMID 36707722 · DOI · PMC10281087
  6. Cadet J, Mouret S, Ravanat JL, Douki T. Photoinduced damage to cellular DNA: direct and photosensitized reactions. Photochem Photobiol. 2012. PMID 22780837 · DOI
  7. Carell T, Burgdorf LT, Kundu LM, Cichon M. The mechanism of action of DNA photolyases. Curr Opin Chem Biol. 2001. PMID 11578921 · DOI
  8. Cadet J, Grand A, Douki T. Solar UV radiation-induced DNA Bipyrimidine photoproducts: formation and mechanistic insights. Top Curr Chem. 2015. PMID 25370518 · DOI
  9. Douki T. The variety of UV-induced pyrimidine dimeric photoproducts in DNA as shown by chromatographic quantification methods. Photochem Photobiol Sci. 2013. PMID 23572060 · DOI
  10. Zhang M, Wang L, Zhong D. Photolyase: Dynamics and electron-transfer mechanisms of DNA repair. Arch Biochem Biophys. 2017. PMID 28802828 · DOI · PMC5650541

About this article

Sources
NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
Verification
Every reference was resolved against PubMed on 2026-10-31; title, year and DOI matched.
Review state
automated source verified; no human expert review has been recorded yet.
Version
1, last updated 2026-10-29.

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At a glance

2,680
PubMed records on this heading
10%
published since 2020
190
review articles
7
randomized trials
10
verified references below

Counts come from PubMed on 2026-10-29; they show how much has been written, not how strong the evidence is.

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