Evidence map›Paper›PMID 19635810›Full record

ArticleMolecular and cellular biology2009

The Saccharomyces cerevisiae Rad6 postreplication repair and Siz1/Srs2 homologous recombination-inhibiting pathways process DNA damage that arises in asf1 mutants.

Ellen S Kats, Jorrit M Enserink, Sandra Martinez, Richard D Kolodner

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

18 citing papers in PubMed, 24 citations in OpenAlex.

  1. Article
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  4. TORC1-dependent sumoylation of Rpc82 promotes RNA polymerase III assembly and activity.Proceedings of the National Academy of Sciences of the United States of America · 2017
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  16. Damage-specific modification of PCNA.Cell cycle (Georgetown, Tex.) · 2010
    Article
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  18. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 2 countries.

Ellen S KatsLudwig Institute for Cancer Research, Departments of Medicine and Cellular and Molecular Medicine, and Biomedical Sciences Graduate Program, UC San Diego School of Medicine, 9500 Gilman Drive, La Jolla, CA 92093-0669, USA.
Jorrit M Enserink
Sandra Martinez
Richard D Kolodner
Ludwig Cancer Research · USUniversity of California, San Diego · US

Funding

ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR01GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard D Kolodner · 1985 to 2026
$10.5M
ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR37GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA SAN DIEGO · PI KOLODNER, RICHARD D · 1992 to 2001
$759k
NIGMS NIH HHS GM26017NIGMS NIH HHS R01 GM026017NIGMS NIH HHS R37 GM026017
6 · The paper itself

Abstract

The Asf1 and Rad6 pathways have been implicated in a number of common processes such as suppression of gross chromosomal rearrangements (GCRs), DNA repair, modification of chromatin, and proper checkpoint functions. We examined the relationship between Asf1 and different gene products implicated in postreplication repair (PRR) pathways in the suppression of GCRs, checkpoint function, sensitivity to hydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of proliferating cell nuclear antigen (PCNA). We found that defects in Rad6 PRR pathway and Siz1/Srs2 homologous recombination suppression (HRS) pathway genes suppressed the increased GCR rates seen in asf1 mutants, which was independent of translesion bypass polymerases but showed an increased dependency on Dun1. Combining an asf1 deletion with different PRR mutations resulted in a synergistic increase in sensitivity to chronic HU and MMS treatment; however, these double mutants were not checkpoint defective, since they were capable of recovering from acute treatment with HU. Interestingly, we found that Asf1 and Rad6 cooperate in ubiquitination of PCNA, indicating that Rad6 and Asf1 function in parallel pathways that ubiquitinate PCNA. Our results show that ASF1 probably contributes to the maintenance of genome stability through multiple mechanisms, some of which involve the PRR and HRS pathways.

Indexed as

DNA RepairRecombination, GeneticCell Cycle ProteinsChromosomes, FungalDNA DamageDNA, FungalDNA HelicasesDNA ReplicationHydroxyureaMethyl MethanesulfonateMolecular ChaperonesMutationProtein Serine-Threonine KinasesSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsS PhaseASF1 protein, S cerevisiaeCell Cycle ProteinsDNA, FungalDNA HelicasesDUN1 protein, S cerevisiaeHydroxyureaMethyl MethanesulfonateMolecular ChaperonesProtein Serine-Threonine KinasesRAD6 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsSiz1 protein, S cerevisiaeSRS2 protein, S cerevisiaeUbiquitin-Conjugating EnzymesUbiquitin-Protein Ligases

Identifiers

PMID19635810
PMCPMC2747975
OpenAlexW2048097625

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.