ArticlePLoS biology2014
Def1 promotes the degradation of Pol3 for polymerase exchange to occur during DNA-damage--induced mutagenesis in Saccharomyces cerevisiae.
Article in PLoS biology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Horizontal gene transfer in Saccharomyces cerevisiae and other Saccharomycotina yeasts: a review.World journal of microbiology & biotechnology · 2026Review
- Structural and functional impact of the POLD1 Ser605del variant in MDPL syndrome: insights from protein-protein interactions.Human genomics · 2025Article
- DEF1: Much more than an RNA polymerase degradation factor.DNA repair · 2021Review
- Article
- The Zn-finger of Saccharomyces cerevisiae Rad18 and its adjacent region mediate interaction with Rad5.G3 (Bethesda, Md.) · 2021Article
- Mechanisms for Maintaining Eukaryotic Replisome Progression in the Presence of DNA Damage.Frontiers in molecular biosciences · 2021Review
- Deletion of the DEF1 gene does not confer UV-immutability but frequently leads to self-diploidization in yeast Saccharomyces cerevisiae.DNA repair · 2018Article
- RNA Polymerase II Transcription Attenuation at the Yeast DNA Repair Gene,G3 (Bethesda, Md.) · 2018Article
- Dependency of Heterochromatin Domains on Replication Factors.G3 (Bethesda, Md.) · 2018Article
- Single-step purification of intrinsic protein complexes inMethodsX · 2018Article
- The translesion DNA polymerases Pol ζ and Rev1 are activated independently of PCNA ubiquitination upon UV radiation in mutants of DNA polymerase δ.PLoS genetics · 2017Article
- Proteomic identification of histone post-translational modifications and proteins enriched at a DNA double-strand break.Nucleic acids research · 2017Article
- 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
- Interaction between the Rev1 C-Terminal Domain and the PolD3 Subunit of Polζ Suggests a Mechanism of Polymerase Exchange upon Rev1/Polζ-Dependent Translesion Synthesis.Biochemistry · 2016Article
- Identifying novel protein phenotype annotations by hybridizing protein-protein interactions and protein sequence similarities.Molecular genetics and genomics : MGG · 2016Article
- Mutations at the Subunit Interface of Yeast Proliferating Cell Nuclear Antigen Reveal a Versatile Regulatory Domain.PloS one · 2016Article
- Genetic instability in budding and fission yeast-sources and mechanisms.FEMS microbiology reviews · 2015Review
- Eukaryotic DNA polymerase ζ.DNA repair · 2015Review
- FF483-484 motif of human Polη mediates its interaction with the POLD2 subunit of Polδ and contributes to DNA damage tolerance.Nucleic acids research · 2015Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
DNA damages hinder the advance of replication forks because of the inability of the replicative polymerases to synthesize across most DNA lesions. Because stalled replication forks are prone to undergo DNA breakage and recombination that can lead to chromosomal rearrangements and cell death, cells possess different mechanisms to ensure the continuity of replication on damaged templates. Specialized, translesion synthesis (TLS) polymerases can take over synthesis at DNA damage sites. TLS polymerases synthesize DNA with a high error rate and are responsible for damage-induced mutagenesis, so their activity must be strictly regulated. However, the mechanism that allows their replacement of the replicative polymerase is unknown. Here, using protein complex purification and yeast genetic tools, we identify Def1 as a key factor for damage-induced mutagenesis in yeast. In in vivo experiments we demonstrate that upon DNA damage, Def1 promotes the ubiquitylation and subsequent proteasomal degradation of Pol3, the catalytic subunit of the replicative polymerase δ, whereas Pol31 and Pol32, the other two subunits of polymerase δ, are not affected. We also show that purified Pol31 and Pol32 can form a complex with the TLS polymerase Rev1. Our results imply that TLS polymerases carry out DNA lesion bypass only after the Def1-assisted removal of Pol3 from the stalled replication fork.
Indexed as
Identifiers
What OpenQuestion holds
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.