Evidence map›Paper›PMID 30206225›Full record

ArticleNature communications2018

The Swr1 chromatin-remodeling complex prevents genome instability induced by replication fork progression defects.

Anjana Srivatsan, Bin-Zhong Li, Barnabas Szakal, Dana Branzei, Christopher D Putnam, Richard D Kolodner

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 21% 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

17 citing papers in PubMed, 22 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Histone H2A variants: Diversifying chromatin to ensure genome integrity.Seminars in cell & developmental biology · 2023
    Review
  5. Article
  6. Article
  7. Histone dynamics during DNA replication stress.Journal of biomedical science · 2021
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. EssentialProceedings of the National Academy of Sciences of the United States of America · 2019
    Article
  16. Article
  17. Review
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 3 institutions in 2 countries.

Anjana SrivatsanLudwig Institute for Cancer Research, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0669, USA.ORCID http://orcid.org/0000-0003-1645-7075
Bin-Zhong LiLudwig Institute for Cancer Research, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0669, USA.
Barnabas SzakalThe FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139, Milan, Italy.ORCID http://orcid.org/0000-0001-6888-1383
Dana BranzeiThe FIRC Institute of Molecular Oncology Foundation, Via Adamello 16, 20139, Milan, Italy.ORCID http://orcid.org/0000-0002-0544-4888
Christopher D PutnamLudwig Institute for Cancer Research, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0669, USA.ORCID http://orcid.org/0000-0002-6145-1265
Richard D KolodnerLudwig Institute for Cancer Research, University of California School of Medicine, San Diego, 9500 Gilman Drive, La Jolla, CA, 92093-0669, USA. rkolodner@ucsd.edu.ORCID http://orcid.org/0000-0002-4806-8384
IFOM · ITLudwig Cancer Research · USUniversity of California San Diego · US

Funding

ENZYMATIC MECHANISMS OF GENETIC RECOMBINATIONR01GM026017 · NIGMS · UNIVERSITY OF CALIFORNIA, SAN DIEGO · PI Richard D Kolodner · 1985 to 2026
$10.5M
NIGMS NIH HHS R01 GM026017
6 · The paper itself

Abstract

Genome instability is associated with tumorigenesis. Here, we identify a role for the histone Htz1, which is deposited by the Swr1 chromatin-remodeling complex (SWR-C), in preventing genome instability in the absence of the replication fork/replication checkpoint proteins Mrc1, Csm3, or Tof1. When combined with deletion of SWR1 or HTZ1, deletion of MRC1, CSM3, or TOF1 or a replication-defective mrc1 mutation causes synergistic increases in gross chromosomal rearrangement (GCR) rates, accumulation of a broad spectrum of GCRs, and hypersensitivity to replication stress. The double mutants have severe replication defects and accumulate aberrant replication intermediates. None of the individual mutations cause large increases in GCR rates; however, defects in MRC1, CSM3 or TOF1 cause activation of the DNA damage checkpoint and replication defects. We propose a model in which Htz1 deposition and retention in chromatin prevents transiently stalled replication forks that occur in mrc1, tof1, or csm3 mutants from being converted to DNA double-strand breaks that trigger genome instability.

Indexed as

Chromatin Assembly and DisassemblyDNA ReplicationGenomic InstabilityAdenosine TriphosphatasesCell CycleChromatinChromosomes, FungalDNA DamageGene RearrangementHomologous RecombinationHydroxyureaModels, BiologicalMutationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsStress, PhysiologicalAdenosine TriphosphatasesChromatinHydroxyureaSaccharomyces cerevisiae ProteinsSwr1 protein, S cerevisiae

Identifiers

PMID30206225
PMCPMC6134005
OpenAlexW2890535025

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.