ArticleDNA repair2017
Def1 and Dst1 play distinct roles in repair of AP lesions in highly transcribed genomic regions.
Article in DNA repair, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- RNAPII Degradation Factor Def1 Is Required for Development, Stress Response, and Full Virulence ofJournal of fungi (Basel, Switzerland) · 2023Article
- Polymerases and DNA Repair in Neurons: Implications in Neuronal Survival and Neurodegenerative Diseases.Frontiers in cellular neuroscience · 2022Review
- DEF1: Much more than an RNA polymerase degradation factor.DNA repair · 2021Review
- DNA damage repair: historical perspectives, mechanistic pathways and clinical translation for targeted cancer therapy.Signal transduction and targeted therapy · 2021Review
- The activity of yeast Apn2 AP endonuclease at uracil-derived AP sites is dependent on the major carbon source.Current genetics · 2021Article
- A Genome-Wide Screen for Genes Affecting Spontaneous Direct-Repeat Recombination inG3 (Bethesda, Md.) · 2020Article
- Nucleotide excision repair of abasic DNA lesions.Nucleic acids research · 2019Article
- Deletion of the DEF1 gene does not confer UV-immutability but frequently leads to self-diploidization in yeast Saccharomyces cerevisiae.DNA repair · 2018Article
- Unscheduled DNA synthesis leads to elevated uracil residues at highly transcribed genomic loci in Saccharomyces cerevisiae.PLoS genetics · 2018Article
- Stimulation of RNA Polymerase II ubiquitination and degradation by yeast mRNA 3'-end processing factors is a conserved DNA damage response in eukaryotes.DNA repair · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Abasic or AP sites generated by spontaneous DNA damage accumulate at a higher rate in actively transcribed regions of the genome in S. cerevisiae and are primarily repaired by base excision repair (BER) pathway. We have demonstrated that transcription-coupled nucleotide excision repair (NER) pathway can functionally replace BER to repair those AP sites located on the transcribed strand much like the strand specific repair of UV-induced pyrimidine dimers. Previous reports indicate that Rad26, a yeast homolog of transcription-repair coupling factor CSB, partly mediates strand-specific repair of UV-dimers as well as AP lesions. Here, we report that Def1, known to promote ubiquitination and degradation of stalled RNA polymerase complex, also directs NER to AP lesions on the transcribed strand of an actively transcribed gene but that its function is dependent on metabolic state of the yeast cells. We additionally show that Dst1, a homolog of mammalian transcription elongation factor TFIIS, interferes with NER-dependent repair of AP lesions while suppressing homologous recombination pathway. Overall, Def1 and Dst1 mediate very different outcomes in response to AP-induced transcription arrest.
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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 OpenQuestion graph.