ArticleThe Journal of biological chemistry2004
Dissecting transcription-coupled and global genomic repair in the chromatin of yeast GAL1-10 genes.
Article in The Journal of biological chemistry, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 55 citations in OpenAlex.
- Interplay of the Tfb1 pleckstrin homology domain with Rad2 and Rad4 in transcription coupled and global genomic nucleotide excision repair.Nucleic acids research · 2024Article
- Transcription as source of genetic heterogeneity in budding yeast.Yeast (Chichester, England) · 2024Review
- Role of Histone Tails and Single Strand DNA Breaks in Nucleosomal Arrest of RNA Polymerase.International journal of molecular sciences · 2023Article
- Article
- Regulation of UV damage repair in quiescent yeast cells.DNA repair · 2020Article
- Histone H4 H75E mutation attenuates global genomic and Rad26-independent transcription-coupled nucleotide excision repair.Nucleic acids research · 2019Article
- Rpb9-deficient cells are defective in DNA damage response and require histone H3 acetylation for survival.Scientific reports · 2018Article
- From Mfd to TRCF and Back Again-A Perspective on Bacterial Transcription-coupled Nucleotide Excision Repair.Photochemistry and photobiology · 2017Review
- Structure of transcribed chromatin is a sensor of DNA damage.Science advances · 2015Article
- DNA repair and recovery of RNA synthesis following exposure to ultraviolet light are delayed in long genes.Nucleic acids research · 2015Article
- Insights into how Spt5 functions in transcription elongation and repressing transcription coupled DNA repair.Nucleic acids research · 2014Article
- Hrq1 facilitates nucleotide excision repair of DNA damage induced by 4-nitroquinoline-1-oxide and cisplatin in Saccharomyces cerevisiae.Journal of microbiology (Seoul, Korea) · 2014Article
- Rad26, the transcription-coupled repair factor in yeast, is required for removal of stalled RNA polymerase-II following UV irradiation.PloS one · 2013Article
- Mechanism of translesion transcription by RNA polymerase II and its role in cellular resistance to DNA damage.Molecular cell · 2012Article
- Diverse roles of RNA polymerase II-associated factor 1 complex in different subpathways of nucleotide excision repair.The Journal of biological chemistry · 2011Article
- How chromatin is remodelled during DNA repair of UV-induced DNA damage in Saccharomyces cerevisiae.PLoS genetics · 2011Article
- Evidence that the histone methyltransferase Dot1 mediates global genomic repair by methylating histone H3 on lysine 79.The Journal of biological chemistry · 2011Article
- Abasic sites in the transcribed strand of yeast DNA are removed by transcription-coupled nucleotide excision repair.Molecular and cellular biology · 2010Article
- The C-terminal repeat domain of Spt5 plays an important role in suppression of Rad26-independent transcription coupled repair.The Journal of biological chemistry · 2010Article
- Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Transcription-coupled repair (TCR) and global genomic repair (GGR) of UV-induced cyclobutane pyrimidine dimers were investigated in the yeast GAL1-10 genes. Both Rpb9- and Rad26-mediated TCR are confined to the transcribed strands, initiating at upstream sites approximately 100 nucleotides from the upstream activating sequence shared by the two genes. However, TCR initiation sites do not correlate with either transcription start sites or TATA boxes. Rad16-mediated GGR tightly correlates with nucleosome positioning when the genes are repressed and are slow in the nucleosome core and fast in linker DNA. Induction of transcription enhanced GGR in nucleosome core DNA, especially in the nucleosomes around and upstream of the transcription start sites. Furthermore, when the genes were induced, GGR was slower in the transcribed regions than in the upstream regions. Finally, simultaneous deletion of RAD16, RAD26, and RPB9 resulted in no detectable repair in all sites along the region analyzed. Our results suggest that (a). TCR may be initiated by a transcription activator, presumably through the loading of RNA polymerase II, rather than by transcription initiation or elongation per se; (b). TCR and nucleosome disruption-enhanced GGR are the major causes of rapid repair in regions around and upstream of transcription start sites; (c). transcription machinery may hinder access of NER factors to a DNA lesion in the absence of a transcription-repair coupling factor; and (d). other than GGR mediated by Rad16 and TCR mediated by Rad26 and Rpb9, no other nucleotide excision repair pathway exists in these RNA polymerase II-transcribed genes.
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