Evidence map›Paper›PMID 15542840›Full record

ArticleMolecular and cellular biology2004

Activation of the DNA damage checkpoint in yeast lacking the histone chaperone anti-silencing function 1.

Christopher Josh Ramey, Susan Howar, Melissa Adkins, Jeffrey Linger, Judson Spicer, Jessica K Tyler

Abstract read
In one paragraph

Article in Molecular and cellular biology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 55 papers.

0numbers the graph read from it
0cells of the map it votes in
55citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

55 citing papers in PubMed, 91 citations in OpenAlex.

  1. Article
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  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Histone modifications as regulators of life and death inMicrobial cell (Graz, Austria) · 2015
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
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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 2 institutions in 1 country.

Christopher Josh RameyDepartment of Biochemistry and Molecular Genetics, University of Colorado Health Sciences Center at Fitzsimons, P.O. Box 6511, Aurora, CO 80045, USA.
Susan Howar
Melissa Adkins
Jeffrey Linger
Judson Spicer
Jessica K Tyler
University of Colorado Health · USUniversity of Colorado Anschutz Medical Campus · US

Funding

Chromatin's Role in Repair of Radiation-induced Damage.R01CA095641 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI TYLER, JESSICA K · 2002 to 2023
$5.2M
Predoctoral Training Program in Molecular BiologyT32GM008730 · NIGMS · UNIVERSITY OF COLORADO DENVER · PI PREKERIS, RYTIS, SCLAFANI, ROBERT A · 1999 to 2019
$3.3M
NCI NIH HHS CA 95641-01NCI NIH HHS R01 CA095641NIGMS NIH HHS T32 GM008730NIGMS NIH HHS T32 GM 08730
6 · The paper itself

Abstract

The packaging of the eukaryotic genome into chromatin is likely to be important for the maintenance of genomic integrity. Chromatin structures are assembled onto newly synthesized DNA by the action of chromatin assembly factors, including anti-silencing function 1 (ASF1). To investigate the role of chromatin structure in the maintenance of genomic integrity, we examined budding yeast lacking the histone chaperone Asf1p. We found that yeast lacking Asf1p accumulate in metaphase of the cell cycle due to activation of the DNA damage checkpoint. Furthermore, yeast lacking Asf1p are highly sensitive to mutations in DNA polymerase alpha and to DNA replicational stresses. Although yeast lacking Asf1p do complete DNA replication, they have greatly elevated rates of DNA damage occurring during DNA replication, as indicated by spontaneous Ddc2p-green fluorescent protein foci. The presence of elevated levels of spontaneous DNA damage in asf1 mutants is due to increased DNA damage, rather than the failure to repair double-strand DNA breaks, because asf1 mutants are fully functional for double-strand DNA repair. Our data indicate that the altered chromatin structure in asf1 mutants leads to elevated rates of spontaneous recombination, mutation, and DNA damage foci formation arising during DNA replication, which in turn activates cell cycle checkpoints that respond to DNA damage.

Indexed as

DNA DamageAdaptor Proteins, Signal TransducingBlotting, WesternCell CycleCell Cycle ProteinsCell DivisionCell ProliferationCell SurvivalChromatinDNADNA-Directed DNA PolymeraseDNA RepairElectrophoresis, Gel, Pulsed-FieldFlow CytometryG2 PhaseGene DeletionAdaptor Proteins, Signal TransducingASF1A protein, humanASF1 protein, S cerevisiaeCell Cycle ProteinsChromatinDNADNA-Directed DNA PolymeraseGreen Fluorescent ProteinsHistonesLCD1 protein, S cerevisiaeMolecular ChaperonesPhosphoproteinsSaccharomyces cerevisiae Proteins

Identifiers

PMID15542840
PMCPMC529054
OpenAlexW2107182018

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.