ArticleDNA repair2017
Stimulation of RNA Polymerase II ubiquitination and degradation by yeast mRNA 3'-end processing factors is a conserved DNA damage response in eukaryotes.
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 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- The yeast checkpoint kinase Mec1p functions in transcription termination by facilitating recruitment of Pcf11p and regulating the torpedo exonuclease Rat1p.Scientific reports · 2025Article
- Article
- Hydroxyurea and inactivation of checkpoint kinase MEC1 inhibit transcription termination and pre-mRNA cleavage at polyadenylation sites in budding yeast.Scientific reports · 2023Article
- A versatile new tool derived from a bacterial deubiquitylase to detect and purify ubiquitylated substrates and their interacting proteins.PLoS biology · 2022Article
- DEF1: Much more than an RNA polymerase degradation factor.DNA repair · 2021Review
- Causes and consequences of RNA polymerase II stalling during transcript elongation.Nature reviews. Molecular cell biology · 2021Review
- Deficiency in classical nonhomologous end-joining-mediated repair of transcribed genes is linked to SCA3 pathogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- A SUMO-dependent pathway controls elongating RNA Polymerase II upon UV-induced damage.Scientific reports · 2019Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The quality and retrieval of genetic information is imperative to the survival and reproduction of all living cells. Ultraviolet (UV) light induces lesions that obstruct DNA access during transcription, replication, and repair. Failure to remove UV-induced lesions can abrogate gene expression and cell division, resulting in permanent DNA mutations. To defend against UV damage, cells utilize transcription-coupled nucleotide excision repair (TC-NER) to quickly target lesions within active genes. In cases of long-term genotoxic stress, a slower alternative pathway promotes degradation of RNA Polymerase II (Pol II) to allow for global genomic nucleotide excision repair (GG-NER). The crosstalk between TC-NER and GG-NER pathways and the extent of their coordination with other nuclear events has remained elusive. We aimed to identify functional links between the DNA damage response (DDR) and the mRNA 3'-end processing complex. Our labs have previously shown that UV-induced inhibition of mRNA processing is a conserved DDR between yeast and mammalian cells. Here we have identified mutations in the yeast mRNA 3'-end processing cleavage factor IA (CFIA) and cleavage and polyadenylation factor (CPF) that confer sensitivity to UV-type DNA damage. In the absence of TC-NER, CFIA and CPF mutants show reduced UV tolerance and an increased frequency of UV-induced genomic mutations, consistent with a role for RNA processing factors in an alternative DNA repair pathway. CFIA and CPF mutants impaired the ubiquitination and degradation of Pol II following DNA damage, but the co-transcriptional recruitment of Pol II degradation factors Elc1 and Def1 was undiminished. Overall these data are consistent with yeast 3'-end processing factors contributing to the removal of Pol II stalled at UV-type DNA lesions, a functional interaction that is conserved between homologous factors in yeast and human cells.
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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.