Evidence map›Paper›PMID 20639887›Full record

ArticleNature structural & molecular biology2010

Replication stress checkpoint signaling controls tRNA gene transcription.

Vesna C Nguyen, Brett W Clelland, Darren J Hockman, Sonya L Kujat-Choy, Holly E Mewhort, Michael C Schultz

Abstract read
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In one paragraph

Article in Nature structural & molecular biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

31 citing papers in PubMed, 45 citations in OpenAlex.

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  20. Regulation of cell death by transfer RNA.Antioxidants & redox signaling · 2013
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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

6 authors at 1 institution in 1 country.

Vesna C NguyenDepartment of Biochemistry, School of Molecular and Systems Medicine, University of Alberta, Edmonton, Alberta, Canada.
Brett W Clelland
Darren J Hockman
Sonya L Kujat-Choy
Holly E Mewhort
Michael C Schultz
University of Alberta · CA

Funding

Canadian Institutes of Health Research
6 · The paper itself

Abstract

In budding yeast, the transcriptional machinery at tRNA genes naturally interferes with replication in a way that can promote chromosome breakage. Here we show that a signaling module composed of core components of the replication stress checkpoint pathway represses this fork-pausing machinery in normally cycling and genotoxin-treated cells. Specifically, the sensor kinase Mec1, the signaling adaptor Mrc1 and the transducer kinase Rad53 relay signals that globally repress tRNA gene transcription during unchallenged proliferation and under conditions of replication stress. Repressive signaling in genotoxin-treated cells requires Rad53-dependent activation of a conserved repressor of tRNA gene transcription, Maf1. Cells lacking Maf1 are sensitive to replication stress under conditions of elevated tRNA gene transcription. We propose that checkpoint control of the fork-pausing activity of tRNA genes complements the repertoire of replisome-targeted mechanisms by which checkpoint proteins promote faithful DNA replication.

Indexed as

Transcription, GeneticCell CycleCell ProliferationDNA ReplicationGenes, FungalMutationRepressor ProteinsRNA Polymerase IIIRNA, TransferSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsSignal TransductionStress, PhysiologicalRepressor ProteinsRNA Polymerase IIIRNA, TransferSaccharomyces cerevisiae Proteins

Identifiers

PMID20639887
OpenAlexW2086031323

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.