Evidence map›Paper›PMID 27017623›Full record

ArticleGenetics2016

DNA Replication Stress Phosphoproteome Profiles Reveal Novel Functional Phosphorylation Sites on Xrs2 in Saccharomyces cerevisiae.

Dongqing Huang, Brian D Piening, Jacob J Kennedy, Chenwei Lin, Corey W Jones-Weinert, Ping Yan, Amanda G Paulovich

Open access · bronzeAbstract read
In one paragraph

Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact, top 99% 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

1 citing paper in PubMed, 3 citations in OpenAlex.

  1. 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

7 authors at 1 institution in 1 country.

Dongqing HuangFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024.
Brian D PieningFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024.
Jacob J KennedyFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024.
Chenwei LinFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024.
Corey W Jones-WeinertFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024.
Ping YanFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024.
Amanda G PaulovichFred Hutchinson Cancer Research Center, Seattle, Washington 98109-1024 apaulovi@fhcrc.org.
Fred Hutch Cancer Center · US

Funding

Phenotype-based approach to find gene interactions underlying breast cancer riskR01CA129604 · NCI · FRED HUTCHINSON CANCER RESEARCH CENTER · PI PAULOVICH, AMANDA G · 2007 to 2011
$1.3M
NCI NIH HHS R01 CA129604
6 · The paper itself

Abstract

In response to replication stress, a phospho-signaling cascade is activated and required for coordination of DNA repair and replication of damaged templates (intra-S-phase checkpoint) . How phospho-signaling coordinates the DNA replication stress response is largely unknown. We employed state-of-the-art liquid chromatography tandem-mass spectrometry (LC-MS/MS) approaches to generate high-coverage and quantitative proteomic and phospho-proteomic profiles during replication stress in yeast, induced by continuous exposure to the DNA alkylating agent methyl methanesulfonate (MMS) . We identified 32,057 unique peptides representing the products of 4296 genes and 22,061 unique phosphopeptides representing the products of 3183 genes. A total of 542 phosphopeptides (mapping to 339 genes) demonstrated an abundance change of greater than or equal to twofold in response to MMS. The screen enabled detection of nearly all of the proteins known to be involved in the DNA damage response, as well as many novel MMS-induced phosphorylations. We assessed the functional importance of a subset of key phosphosites by engineering a panel of phosphosite mutants in which an amino acid substitution prevents phosphorylation. In total, we successfully mutated 15 MMS-responsive phosphorylation sites in seven representative genes including APN1 (base excision repair); CTF4 and TOF1 (checkpoint and sister-chromatid cohesion); MPH1 (resolution of homologous recombination intermediates); RAD50 and XRS2 (MRX complex); and RAD18 (PRR). All of these phosphorylation site mutants exhibited MMS sensitivity, indicating an important role in protecting cells from DNA damage. In particular, we identified MMS-induced phosphorylation sites on Xrs2 that are required for MMS resistance in the absence of the MRX activator, Sae2, and that affect telomere maintenance.

Indexed as

DNA ReplicationProtein Processing, Post-TranslationalStress, PhysiologicalAmino Acid MotifsDNA-Binding ProteinsDNA Repair EnzymesEndodeoxyribonucleasesPhosphorylationProteomeSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsApn1 protein, S cerevisiaeCTF4 protein, S cerevisiaeDNA-Binding ProteinsDNA Repair EnzymesEndodeoxyribonucleasesProteomeRAD50 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTOF1 protein, S cerevisiaeXRS2 protein, S cerevisiaeDNA damage checkpointDNA damage responsegenetic interactionhomologous recombinationmass spectrometrymethyl methanesulfonatephosphorylationtelomere

Identifiers

PMID27017623
PMCPMC4858785
OpenAlexW2307842355

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.