ArticleNAR genomics and bioinformatics2021
Exons and introns exhibit transcriptional strand asymmetry of dinucleotide distribution, damage formation and DNA repair.
Article in NAR genomics and bioinformatics, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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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.
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.
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Who cites it
9 citing papers in PubMed, 12 citations in OpenAlex.
- DREAM repressive activity links somatic mutation, lifespan and disease.Nature aging · 2026Article
- Conserved 3D genome reorganization during DNA repair.Life science alliance · 2026Review
- The DREAM complex links somatic mutation, lifespan, and disease.bioRxiv : the preprint server for biology · 2025Article
- The epigenetic landscape shapes smoking-induced mutagenesis by modulating DNA damage susceptibility and repair efficiency.Nucleic acids research · 2025Article
- STK19 is a transcription-coupled repair factor that participates in UVSSA ubiquitination and TFIIH loading.Nucleic acids research · 2024Article
- ASH1L guards cis-regulatory elements against cyclobutane pyrimidine dimer induction.Nucleic acids research · 2024Article
- Gene architecture is a determinant of the transcriptional response to bulky DNA damages.Life science alliance · 2024Article
- Strand asymmetries across genomic processes.Computational and structural biotechnology journal · 2023Review
- Set2 histone methyltransferase regulates transcription coupled-nucleotide excision repair in yeast.PLoS genetics · 2022Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Recent cancer sequencing efforts have uncovered asymmetry in DNA damage induced mutagenesis between the transcribed and non-transcribed strands of genes. Here, we investigate the major type of damage induced by ultraviolet (UV) radiation, the cyclobutane pyrimidine dimers (CPDs), which are formed primarily in TT dinucleotides. We reveal that a transcriptional asymmetry already exists at the level of TT dinucleotide frequency and therefore also in CPD damage formation. This asymmetry is conserved in vertebrates and invertebrates and is completely reversed between introns and exons. We show the asymmetry in introns is linked to the transcription process itself, and is also found in enhancer elements. In contrast, the asymmetry in exons is not correlated to transcription, and is associated with codon usage preferences. Reanalysis of nucleotide excision repair, normalizing repair to the underlying TT frequencies, we show repair of CPDs is more efficient in exons compared to introns, contributing to the maintenance and integrity of coding regions. Our results highlight the importance of considering the primary sequence of the DNA in determining DNA damage sensitivity and mutagenic potential.
Identifiers
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Registered trials
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 Socratic graph.