Evidence map›Paper›PMID 27457959›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2016

Chromosomal landscape of UV damage formation and repair at single-nucleotide resolution.

Peng Mao, Michael J Smerdon, Steven A Roberts, John J Wyrick

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers.

0numbers the graph read from it
0cells of the map it votes in
115citing papers in PubMed
9.2field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

115 citing papers in PubMed, 161 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Nanorate sequencing reveals theProceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

55 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 1 institution in 1 country.

Peng MaoSchool of Molecular Biosciences, Washington State University, Pullman, WA 99164;
Michael J SmerdonSchool of Molecular Biosciences, Washington State University, Pullman, WA 99164;
Steven A RobertsSchool of Molecular Biosciences, Washington State University, Pullman, WA 99164;
John J WyrickSchool of Molecular Biosciences, Washington State University, Pullman, WA 99164; Center for Reproductive Biology, Washington State University, Pullman, WA 99164 jwyrick@vetmed.wsu.edu.
Washington State University · US

Funding

Repair of Carcinogen Damaged DNA in Human ChromatinR37ES002614 · NIEHS · WASHINGTON STATE UNIVERSITY · PI SMERDON, MICHAEL J · 2001 to 2010
$4.0M
REPAIR OF CARCINOGEN-DAMAGED DNA IN HUMAN CHROMATINR01ES002614 · NIEHS · WASHINGTON STATE UNIVERSITY · PI SMERDON, MICHAEL J, WYRICK, JOHN J · 1985 to 2015
$2.5M
Environmentally-modulated cytosine deamination in genome instability and cancerR00ES022633 · NIEHS · WASHINGTON STATE UNIVERSITY · PI ROBERTS, STEVEN A · 2015 to 2017
$868k
NIEHS NIH HHS R00 ES022633NIEHS NIH HHS R01 ES002614NIEHS NIH HHS R37 ES002614
6 · The paper itself

Abstract

UV-induced DNA lesions are important contributors to mutagenesis and cancer, but it is not fully understood how the chromosomal landscape influences UV lesion formation and repair. Genome-wide profiling of repair activity in UV irradiated cells has revealed significant variations in repair kinetics across the genome, not only among large chromatin domains, but also at individual transcription factor binding sites. Here we report that there is also a striking but predictable variation in initial UV damage levels across a eukaryotic genome. We used a new high-throughput sequencing method, known as CPD-seq, to precisely map UV-induced cyclobutane pyrimidine dimers (CPDs) at single-nucleotide resolution throughout the yeast genome. This analysis revealed that individual nucleosomes significantly alter CPD formation, protecting nucleosomal DNA with an inward rotational setting, even though such DNA is, on average, more intrinsically prone to form CPD lesions. CPD formation is also inhibited by DNA-bound transcription factors, in effect shielding important DNA elements from UV damage. Analysis of CPD repair revealed that initial differences in CPD damage formation often persist, even at later repair time points. Furthermore, our high-resolution data demonstrate, to our knowledge for the first time, that CPD repair is significantly less efficient at translational positions near the dyad of strongly positioned nucleosomes in the yeast genome. These findings define the global roles of nucleosomes and transcription factors in both UV damage formation and repair, and have important implications for our understanding of UV-induced mutagenesis in human cancers.

Indexed as

DNA DamageDNA RepairUltraviolet RaysBinding SitesHeterochromatinHigh-Throughput Nucleotide SequencingNucleosomesPyrimidine DimersTranscription FactorsHeterochromatinNucleosomesPyrimidine DimersTranscription FactorschromatinDNA damageDNA repairnucleosometranscription factor

Identifiers

PMID27457959
PMCPMC4987812
OpenAlexW2505939414

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.