Evidence map›Paper›PMID 25894965›Full record

ArticlePLoS genetics2015

Ndd1 turnover by SCF(Grr1) is inhibited by the DNA damage checkpoint in Saccharomyces cerevisiae.

Ellen R Edenberg, Kevin G Mark, David P Toczyski

Open access · goldAbstract read
In one paragraph

Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
0.6field-weighted citation impact, top 32% 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

7 citing papers in PubMed, 13 citations in OpenAlex.

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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

3 authors at 1 institution in 1 country.

Ellen R EdenbergDepartment of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, California, United States of America.
Kevin G MarkDepartment of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, California, United States of America.
David P ToczyskiDepartment of Biochemistry and Biophysics, University of California, San Francisco, San Francisco, California, United States of America.
University of California, San Francisco · US

Funding

Regulation by post-translation modifications in response to stressR35GM118104 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TOCZYSKI, DAVID PAUL · 2016 to 2025
$7.2M
Regulation and Targets of the DNA Damage CheckpointR01GM059691 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TOCZYSKI, DAVID PAUL · 1999 to 2015
$5.8M
Structure and function of the APCR01GM070539 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI TOCZYSKI, DAVID PAUL · 2004 to 2015
$3.9M
NIGMS NIH HHS GM059691NIGMS NIH HHS GM070539NIGMS NIH HHS R01 GM059691NIGMS NIH HHS R01 GM070539NIGMS NIH HHS R35 GM118104
6 · The paper itself

Abstract

In Saccharomyces cerevisiae, Ndd1 is the dedicated transcriptional activator of the mitotic gene cluster, which includes thirty-three genes that encode key mitotic regulators, making Ndd1 a hub for the control of mitosis. Previous work has shown that multiple kinases, including cyclin-dependent kinase (Cdk1), phosphorylate Ndd1 to regulate its activity during the cell cycle. Previously, we showed that Ndd1 was inhibited by phosphorylation in response to DNA damage. Here, we show that Ndd1 is also subject to regulation by protein turnover during the mitotic cell cycle: Ndd1 is unstable during an unperturbed cell cycle, but is strongly stabilized in response to DNA damage. We find that Ndd1 turnover in metaphase requires Cdk1 activity and the ubiquitin ligase SCF(Grr1). In response to DNA damage, Ndd1 stabilization requires the checkpoint kinases Mec1/Tel1 and Swe1, the S. cerevisiae homolog of the Wee1 kinase. In both humans and yeast, the checkpoint promotes Wee1-dependent inhibitory phosphorylation of Cdk1 following exposure to DNA damage. While this is critical for checkpoint-induced arrest in most organisms, this is not true in budding yeast, where the function of damage-induced inhibitory phosphorylation is less well understood. We propose that the DNA damage checkpoint stabilizes Ndd1 by inhibiting Cdk1, which we show is required for targeting Ndd1 for destruction.

Indexed as

CDC2 Protein KinaseCell CycleCell Cycle ProteinsDNA DamageF-Box ProteinsGene Expression Regulation, FungalHumansIntracellular Signaling Peptides and ProteinsMitosisSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsUbiquitin-Protein LigasesCDC2 Protein KinaseCell Cycle ProteinsF-Box ProteinsGRR1 protein, S cerevisiaeIntracellular Signaling Peptides and ProteinsNDD1 protein, S cerevisiaeRAD24 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTranscription FactorsUbiquitin-Protein Ligases

Identifiers

PMID25894965
PMCPMC4403921
OpenAlexW2086871074

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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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.