Evidence map›Paper›PMID 30590694›Full record

ArticleNucleic acids research2019

DNA Ligase 1 is an essential mediator of sister chromatid telomere fusions in G2 cell cycle phase.

Kate Liddiard, Brian Ruis, Yinan Kan, Kez Cleal, Kevin E Ashelford, Eric A Hendrickson, Duncan M Baird

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

21 citing papers in PubMed, 28 citations in OpenAlex.

  1. Article
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  11. Mechanistic origins of diverse genome rearrangements in cancer.Seminars in cell & developmental biology · 2022
    Review
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Telomere fusions and translocations: a bridge too far?Current opinion in genetics & development · 2020
    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

7 authors at 2 institutions in 2 countries.

Kate LiddiardDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Brian RuisDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Yinan KanDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Kez ClealDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Kevin E AshelfordDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Eric A HendricksonDepartment of Biochemistry, Molecular Biology, and Biophysics, University of Minnesota, Minneapolis, MN 55455, USA.
Duncan M BairdDivision of Cancer and Genetics, School of Medicine, Cardiff University, Heath Park, Cardiff CF14 4XN, UK.
Cardiff University · GBUniversity of Minnesota · US

Funding

Women's CancerP30CA077598 · NCI · UNIVERSITY OF MINNESOTA TWIN CITIES · PI Timothy C. Hallstrom · 1998 to 2026
$100.4M
The mechanism of Cas9/CRISPR-initiated genome modification in human somatic cellsR01GM088351 · NIGMS · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2010 to 2018
$2.3M
Ligase III regulates survival from crisis induced by gradual telomere shorteningR01CA190492 · NCI · UNIVERSITY OF MINNESOTA · PI HENDRICKSON, ERIC A · 2015 to 2019
$1.7M
Cancer Research UK 18246NCI NIH HHS P30 CA077598NCI NIH HHS R01 CA190492NIGMS NIH HHS R01 GM088351
6 · The paper itself

Abstract

Fusion of critically short or damaged telomeres is associated with the genomic rearrangements that support malignant transformation. We have demonstrated the fundamental contribution of DNA ligase 4-dependent classical non-homologous end-joining to long-range inter-chromosomal telomere fusions. In contrast, localized genomic recombinations initiated by sister chromatid fusion are predominantly mediated by alternative non-homologous end-joining activity that may employ either DNA ligase 3 or DNA ligase 1. In this study, we sought to discriminate the relative involvement of these ligases in sister chromatid telomere fusion through a precise genetic dissociation of functional activity. We have resolved an essential and non-redundant role for DNA ligase 1 in the fusion of sister chromatids bearing targeted double strand DNA breaks that is entirely uncoupled from its requisite engagement in DNA replication. Importantly, this fusogenic repair occurs in cells fully proficient for non-homologous end-joining and is not compensated by DNA ligases 3 or 4. The dual functions of DNA ligase 1 in replication and non-homologous end-joining uniquely position and capacitate this ligase for DNA repair at stalled replication forks, facilitating mitotic progression.

Indexed as

ChromatidsDNA Breaks, Double-StrandedDNA End-Joining RepairDNA Ligase ATPDNA RepairDNA ReplicationG2 Phase Cell Cycle CheckpointsHCT116 CellsHumansMitosisPoly-ADP-Ribose Binding ProteinsSister Chromatid ExchangeTelomereDNA Ligase ATPLIG3 protein, humanPoly-ADP-Ribose Binding Proteins

Identifiers

PMID30590694
PMCPMC6411840
OpenAlexW2905934322

What OpenQuestion holds

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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.