Evidence map›Paper›PMID 27222517›Full record

ArticleGenes & development2016

Asf1 facilitates dephosphorylation of Rad53 after DNA double-strand break repair.

Michael Tsabar, David P Waterman, Fiona Aguilar, Lizabeth Katsnelson, Vinay V Eapen, Gonen Memisoglu, James E Haber

Open access · diamondAbstract read
In one paragraph

Article in Genes & development, 2016. 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
–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

18 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
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  10. Novel insights into the mechanism of cell cycle kinases Mec1(ATR) and Tel1(ATM).Critical reviews in biochemistry and molecular biology · 2021
    Article
  11. Review
  12. Mec1Cell reports · 2019
    Article
  13. Article
  14. Review
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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

7 authors at 1 institution in 1 country.

Michael TsabarDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
David P WatermanDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
Fiona AguilarDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
Lizabeth KatsnelsonDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
Vinay V EapenDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
Gonen MemisogluDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
James E HaberDepartment of Biology, Rosenstiel Basic Medical Sciences Research Center, Brandeis University, Waltham, Massachusetts 02454, USA.
Brandeis University · US

Funding

GENETIC AND BIOCHEMICAL MECHANISMS OF REGULATIONT32GM007122 · NIGMS · BRANDEIS UNIVERSITY · PI LOVETT, SUSAN THOMAS · 1985 to 2020
$7.5M
Recombination Mechanisms in Yeast Cell DifferentiationR37GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2007 to 2016
$5.5M
Arrest, Recovery, and Adaptation from DNA DamageR01GM061766 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 2001 to 2016
$4.6M
RECOMBINATION MECHANISMS IN YEAST CELL DIFFERENTIATIONR01GM020056 · NIGMS · BRANDEIS UNIVERSITY · PI HABER, JAMES E · 1985 to 2006
$3.4M
NIGMS NIH HHS R01 GM020056NIGMS NIH HHS R01 GM061766NIGMS NIH HHS R37 GM020056NIGMS NIH HHS T32 GM007122
6 · The paper itself

Abstract

To allow for sufficient time to repair DNA double-stranded breaks (DSBs), eukaryotic cells activate the DNA damage checkpoint. In budding yeast, Rad53 (mammalian Chk2) phosphorylation parallels the persistence of the unrepaired DSB and is extinguished when repair is complete in a process termed recovery or when the cells adapt to the DNA damage checkpoint. A strain containing a slowly repaired DSB does not require the histone chaperone Asf1 to resume cell cycle progression after DSB repair. When a second, rapidly repairable DSB is added to this strain, Asf1 becomes required for recovery. Recovery from two repairable DSBs also depends on the histone acetyltransferase Rtt109 and the cullin subunit Rtt101, both of which modify histone H3 that is associated with Asf1. We show that dissociation of histone H3 from Asf1 is required for efficient recovery and that Asf1 is required for complete dephosphorylation of Rad53 when the upstream DNA damage checkpoint signaling is turned off. Our data suggest that the requirements for recovery from the DNA damage checkpoint become more stringent with increased levels of damage and that Asf1 plays a histone chaperone-independent role in facilitating complete Rad53 dephosphorylation following repair.

Indexed as

DNA Breaks, Double-StrandedDNA RepairCell Cycle CheckpointsCell Cycle ProteinsCheckpoint Kinase 2Cullin ProteinsHistone AcetyltransferasesHistonesMolecular ChaperonesPhosphorylationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsASF1 protein, S cerevisiaeCell Cycle ProteinsCheckpoint Kinase 2Cullin ProteinsHistone AcetyltransferasesHistonesMolecular ChaperonesRAD53 protein, S cerevisiaeRTT101 protein, S cerevisiaeRtt109 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsAsf1DNA damage checkpointDNA double-stranded breaksRad53Rtt101Rtt109

Identifiers

PMID27222517
PMCPMC4888841
OpenAlexW2404455434

What OpenQuestion holds

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LicenceCC BY-NC
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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.