ArticleNucleic acids research2002
Transcription elongation factor Spt4 mediates loss of phosphorylated RNA polymerase II transcription in response to DNA damage.
Article in Nucleic acids research, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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.
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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
5 citing papers in PubMed, 15 citations in OpenAlex.
- NusG-Spt5 Transcription Factors: Universal, Dynamic Modulators of Gene Expression.Journal of molecular biology · 2025Review
- Suppressor of Ty homolog-5, a novel tumor-specific human telomerase reverse transcriptase promoter-binding protein and activator in colon cancer cells.Oncotarget · 2015Article
- The Spt4-Spt5 complex: a multi-faceted regulator of transcription elongation.Biochimica et biophysica acta · 2013Review
- Rad26p, a transcription-coupled repair factor, is recruited to the site of DNA lesion in an elongating RNA polymerase II-dependent manner in vivo.Nucleic acids research · 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
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previously, we found that Rad26, the yeast Cockayne syndrome B homolog and the transcription elongation factor Spt4 mediate transcription-coupled repair of UV-induced DNA damage. Here we studied the effect of DNA damage on transcription by directly analyzing the RNA polymerase II localization at active genes in vivo. A rad26 defect leads to loss of Ser5 phosphorylated RNA polymerase II localization to active genes, while localization is only transiently diminished in wild type cells. In contrast, loss of Ser5-P RNAP II localization is suppressed in spt4 cells. Interestingly, even when DNA damage is persistent the absence of Spt4 leads to a delayed loss of transcription suggesting that Spt4 is directly involved in mediating transcription shutdown. Comparative analysis of phosphorylated and non-phosphorylated RNA polymerase II localization revealed that Ser5-P RNAP II is preferentially lost in the presence of DNA damage. In addition, we found evidence for a transient Rad26 localization to active genes in response to DNA damage. These findings provide insight into the transcriptional response to DNA damage and the factors involved in communicating this response, which has direct implications for our understanding of transcription-repair coupling.
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Registered trials
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