Evidence map›Paper›PMID 39656839›Full record

ArticleeLife2024

Prolonged cell cycle arrest in response to DNA damage in yeast requires the maintenance of DNA damage signaling and the spindle assembly checkpoint.

Felix Y Zhou, David P Waterman, Marissa Ashton, Suhaily Caban-Penix, Gonen Memisoglu, Vinay V Eapen, James E Haber

Abstract read
In one paragraph

Article in eLife, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
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

8 citing papers in PubMed.

  1. [Mefloquine HCl promotes DNA repair and alleviates radiation-induced lung epithelial cell injury].Nan fang yi ke da xue xue bao = Journal of Southern Medical University · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors.

Felix Y Zhou *Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.ORCID https://orcid.org/0000-0002-8619-7160
David P Waterman *Department of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.
Marissa AshtonDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.
Suhaily Caban-PenixDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.
Gonen MemisogluDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.
Vinay V EapenDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.
James E HaberDepartment of Biology and Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, United States.ORCID https://orcid.org/0000-0002-1878-0610

Funding

DNA Damage Response and Repair of a Broken ChromosomeR35GM127029 · NIGMS · BRANDEIS UNIVERSITY · PI JAMES E HABER · 2018 to 2026
$8.6M
GENETIC AND BIOCHEMICAL MECHANISMS OF REGULATIONT32GM007122 · NIGMS · BRANDEIS UNIVERSITY · PI LOVETT, SUSAN THOMAS · 1985 to 2020
$7.5M
Predoctoral Training in Cross-Disciplinary Molecular and Cellular BiologyT32GM139798 · NIGMS · BRANDEIS UNIVERSITY · PI Paul Garrity, Bruce L Goode · 2021 to 2026
$3.5M
Elucidating the mechanisms of non-canonical CDK8 function in DNA damage signalingF32GM145156 · NIGMS · UNIVERSITY OF CHICAGO · PI MEMISOGLU, GONEN · 2022 to 2023
$144k
NIGMS NIH HHS 5T32GM139798NIGMS NIH HHS F32 GM145156NIGMS NIH HHS R35 GM127029NIGMS NIH HHS T32 GM007122NIGMS NIH HHS T32 GM139798NIH HHS F32-GM145156NIH HHS R35 GM127029NIH HHS TM32GM007122
6 · The paper itself

Abstract

Cells evoke the DNA damage checkpoint (DDC) to inhibit mitosis in the presence of DNA double-strand breaks (DSBs) to allow more time for DNA repair. In budding yeast, a single irreparable DSB is sufficient to activate the DDC and induce cell cycle arrest prior to anaphase for about 12-15 hr, after which cells 'adapt' to the damage by extinguishing the DDC and resuming the cell cycle. While activation of the DNA damage-dependent cell cycle arrest is well understood, how it is maintained remains unclear. To address this, we conditionally depleted key DDC proteins after the DDC was fully activated and monitored changes in the maintenance of cell cycle arrest. Degradation of Ddc2

Indexed as

Cell Cycle CheckpointsCell Cycle ProteinsDNA DamageSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsM Phase Cell Cycle CheckpointsSignal TransductionCell Cycle ProteinsSaccharomyces cerevisiae Proteinsauxin-inducible degronchromosomesDDCDNA damage checkpointdouble-strand breakDSBgene expressionHO endonucleaseSACS. cerevisiaeS. cerevisiae budding yeastspindle assembly 3 checkpoint

Identifiers

PMID39656839
PMCPMC11630823

What OpenQuestion holds

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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.