Evidence map›Paper›PMID 31636207›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

Deletions associated with stabilization of the Top1 cleavage complex in yeast are products of the nonhomologous end-joining pathway.

Jang-Eun Cho, Sue Jinks-Robertson

Open access · hybridAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 1 pooled it
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

13 citing papers in PubMed, 1 synthesis or guideline pooled it, 21 citations in OpenAlex.

  1. Pooled it
  2. Genome Instability Induced by Topoisomerase Misfunction.International journal of molecular sciences · 2024
    Review
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Replication-independent instability of Friedreich's ataxia GAA repeats during chronological aging.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  11. Review
  12. Article
  13. 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

2 authors at 1 institution in 1 country.

Jang-Eun ChoDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710.
Sue Jinks-RobertsonDepartment of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, NC 27710 sue.robertson@duke.edu.ORCID 0000-0001-5924-5852
Duke Medical Center · US

Funding

Women's Cancer Research ProgramP30CA014236 · NCI · DUKE UNIVERSITY · PI JOHN N. NORTON · 1985 to 2026
$174.8M
Regulation of mitotic genome stability in yeast.R35GM118077 · NIGMS · DUKE UNIVERSITY · PI JINKS-ROBERTSON, SUE · 2016 to 2023
$4.5M
NCI NIH HHS P30 CA014236NIGMS NIH HHS R35 GM118077
6 · The paper itself

Abstract

Topoisomerase I (Top1) resolves supercoils by nicking one DNA strand and facilitating religation after torsional stress has been relieved. During its reaction cycle, Top1 forms a covalent cleavage complex (Top1cc) with the nicked DNA, and this intermediate can be converted into a toxic double-strand break (DSB) during DNA replication. We previously reported that Top1cc trapping in yeast increases DSB-independent, short deletions at tandemly repeated sequences. In the current study, we report a type of DSB-dependent mutation associated with Top1cc stabilization: large deletions (median size, ∼100 bp) with little or no homology at deletion junctions. Genetic analyses demonstrated that Top1cc-dependent large deletions are products of the nonhomologous end-joining (NHEJ) pathway and require Top1cc removal from DNA ends. Furthermore, these events accumulated in quiescent cells, suggesting that the causative DSBs may arise outside the context of replication. We propose a model in which the ends of different, Top1-associated DSBs are joined via NHEJ, which results in deletion of the intervening sequence. These findings have important implications for understanding the mutagenic effects of chemotherapeutic drugs that stabilize the Top1cc.

Indexed as

DNA End-Joining RepairSequence DeletionDNA Breaks, Double-StrandedDNA, FungalDNA ReplicationDNA Topoisomerases, Type IModels, BiologicalSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsDNA, FungalDNA Topoisomerases, Type ISaccharomyces cerevisiae Proteinsdouble-strand breaknonhomologous end joiningtopoisomerase Iyeast

Identifiers

PMID31636207
PMCPMC6842612
OpenAlexW2981511141

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.