Evidence map›Paper›PMID 28049846›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

SIR2 suppresses replication gaps and genome instability by balancing replication between repetitive and unique sequences.

Eric J Foss, Uyen Lao, Emily Dalrymple, Robin L Adrianse, Taylor Loe, Antonio Bedalov

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
2.8field-weighted citation impact, top 9% 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

25 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Review
  8. Article
  9. Review
  10. Sir2 takes affirmative action to ensure equal opportunity in replication origin licensing.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  11. Sir2 mitigates an intrinsic imbalance in origin licensing efficiency between early- and late-replicating euchromatin.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  12. Article
  13. Article
  14. Review
  15. Article
  16. The peculiar genetics of the ribosomal DNA blurs the boundaries of transgenerational epigenetic inheritance.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Review
  17. Ribosomal DNA instability and genome adaptability.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2019
    Review
  18. Review
  19. Article
  20. Article
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.

Eric J FossDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.
Uyen LaoDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.
Emily DalrympleDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.
Robin L AdrianseDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.
Taylor LoeDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109.
Antonio BedalovDivision of Clinical Research, Fred Hutchinson Cancer Research Center, Seattle, WA 98109; abedalov@fredhutch.org.
Fred Hutch Cancer Center · USUniversity of Washington · US

Funding

Origin firing at repetitive sequences and genome replication - Admin SupplementR01GM117446 · NIGMS · FRED HUTCHINSON CANCER RESEARCH CENTER · PI BEDALOV, ANTONIO · 2016 to 2023
$4.3M
NIGMS NIH HHS R01 GM117446
6 · The paper itself

Abstract

Replication gaps that persist into mitosis likely represent important threats to genome stability, but experimental identification of these gaps has proved challenging. We have developed a technique that allows us to explore the dynamics by which genome replication is completed before mitosis. Using this approach, we demonstrate that excessive allocation of replication resources to origins within repetitive regions, induced by SIR2 deletion, leads to persistent replication gaps and genome instability. Conversely, the weakening of replication origins in repetitive regions suppresses these gaps. Given known age- and cancer-associated changes in chromatin accessibility at repetitive sequences, we suggest that replication gaps resulting from misallocation of replication resources underlie age- and disease-associated genome instability.

Indexed as

DNA ReplicationGenomic InstabilityChromosomes, FungalDNA, FungalDNA, RibosomalGene DeletionGenome, FungalHumansModels, BiologicalRepetitive Sequences, Nucleic AcidReplication OriginSilent Information Regulator Proteins, Saccharomyces cerevisiaeSirtuin 2DNA, FungalDNA, RibosomalSilent Information Regulator Proteins, Saccharomyces cerevisiaeSIR2 protein, S cerevisiaeSirtuin 2DNA replicationrepetitive sequencesreplication gapsribosomal DNASIR2

Identifiers

PMID28049846
PMCPMC5255580
OpenAlexW2563271003

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.