ArticleGenetics2000
The Saccharomyces cerevisiae RAD6 group is composed of an error-prone and two error-free postreplication repair pathways.
Article in Genetics, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 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
66 citing papers in PubMed, 156 citations in OpenAlex.
- Article
- Temporally distinct post-replicative repair mechanisms fill PRIMPOL-dependent ssDNA gaps in human cells.Molecular cell · 2021Article
- To skip or not to skip: choosing repriming to tolerate DNA damage.Molecular cell · 2021Review
- Distinct requirements for budding yeast Rev1 and Polη in translesion DNA synthesis across different types of DNA damage.Current genetics · 2020Article
- The Ubiquitin Conjugating Enzyme: An Important Ubiquitin Transfer Platform in Ubiquitin-Proteasome System.International journal of molecular sciences · 2020Review
- Repair of base damage within break-induced replication intermediates promotes kataegis associated with chromosome rearrangements.Nucleic acids research · 2019Article
- Rad5 dysregulation drives hyperactive recombination at replication forks resulting in cisplatin sensitivity and genome instability.Nucleic acids research · 2019Article
- Review
- Characterization of four rice UEV1 genes required for Lys63-linked polyubiquitination and distinct functions.BMC plant biology · 2017Article
- Avoidance of APOBEC3B-induced mutation by error-free lesion bypass.Nucleic acids research · 2017Article
- Genome maintenance in Saccharomyces cerevisiae: the role of SUMO and SUMO-targeted ubiquitin ligases.Nucleic acids research · 2017Review
- Mechanisms of Post-Replication DNA Repair.Genes · 2017Review
- Ubc13: the Lys63 ubiquitin chain building machine.Oncotarget · 2016Review
- Involvement of budding yeast Rad5 in translesion DNA synthesis through physical interaction with Rev1.Nucleic acids research · 2016Article
- The Regulation of DNA Damage Tolerance by Ubiquitin and Ubiquitin-Like Modifiers.Frontiers in genetics · 2016Review
- Regulation of translesion DNA synthesis: Posttranslational modification of lysine residues in key proteins.DNA repair · 2015Review
- Article
- Protein ubiquitination in lymphoid malignancies.Immunological reviews · 2015Review
- Length-dependent processing of telomeres in the absence of telomerase.Nucleic acids research · 2014Article
- Review
6 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RAD6 postreplication repair and mutagenesis pathway is the only major radiation repair pathway yet to be extensively characterized. It has been previously speculated that the RAD6 pathway consists of two parallel subpathways, one error free and another error prone (mutagenic). Here we show that the RAD6 group genes can be exclusively divided into three rather than two independent subpathways represented by the RAD5, POL30, and REV3 genes; the REV3 pathway is largely mutagenic, whereas the RAD5 and the POL30 pathways are deemed error free. Mutants carrying characteristic mutations in each of the three subpathways are phenotypically indistinguishable from a single mutant such as rad18, which is defective in the entire RAD6 postreplication repair/tolerance pathway. Furthermore, the rad18 mutation is epistatic to all single or combined mutations in any of the above three subpathways. Our data also suggest that MMS2 and UBC13 play a key role in coordinating the response of the error-free subpathways; Mms2 and Ubc13 form a complex required for a novel polyubiquitin chain assembly, which probably serves as a signal transducer to promote both RAD5 and POL30 error-free postreplication repair pathways. The model established by this study will facilitate further research into the molecular mechanisms of postreplication repair and translesion DNA synthesis. In view of the high degree of sequence conservation of the RAD6 pathway genes among all eukaryotes, the model presented in this study may also apply to mammalian cells and predicts links to human diseases.
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.