Evidence map›Paper›PMID 33264397›Full record

ArticleNucleic acids research2020

Interstitial telomere sequences disrupt break-induced replication and drive formation of ectopic telomeres.

Elizabeth A Stivison, Kati J Young, Lorraine S Symington

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 25% 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, 15 citations in OpenAlex.

  1. Article
  2. Article
  3. Mechanisms and genomic implications of break-induced replication.Nature structural & molecular biology · 2025
    Review
  4. Review
  5. Article
  6. Chromosomal conservatism vs chromosomal megaevolution: enigma of karyotypic evolution in Lepidoptera.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2023
    Article
  7. Article
  8. Break-induced replication: unraveling each step.Trends in genetics : TIG · 2022
    Review
  9. Article
  10. Review
  11. Break-induced replication mechanisms in yeast and mammals.Current opinion in genetics & development · 2021
    Review
  12. Homologous recombination within repetitive DNA.Current opinion in genetics & development · 2021
    Review
  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

3 authors at 1 institution in 1 country.

Elizabeth A StivisonProgram in Nutritional and Metabolic Biology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Kati J YoungDepartment of Microbiology and Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Lorraine S SymingtonDepartment of Microbiology and Immunology, Columbia University Irving Medical Center, New York, NY 10032, USA.
Columbia University Irving Medical Center · US

Funding

Mechanism and regulation of DNA double-strand break repairR35GM126997 · NIGMS · COLUMBIA UNIVERSITY HEALTH SCIENCES · PI Lorraine S Symington · 2018 to 2026
$5.9M
NIGMS NIH HHS R35 GM126997
6 · The paper itself

Abstract

Break-induced replication (BIR) is a mechanism used to heal one-ended DNA double-strand breaks, such as those formed at collapsed replication forks or eroded telomeres. Instead of utilizing a canonical replication fork, BIR is driven by a migrating D-loop and is associated with a high frequency of mutagenesis. Here we show that when BIR encounters an interstitial telomere sequence (ITS), the machinery frequently terminates, resulting in the formation of an ectopic telomere. The primary mechanism to convert the ITS to a functional telomere is by telomerase-catalyzed addition of telomeric repeats with homology-directed repair serving as a back-up mechanism. Termination of BIR and creation of an ectopic telomere is promoted by Mph1/FANCM helicase, which has the capacity to disassemble D-loops. Other sequences that have the potential to seed new telomeres but lack the unique features of a natural telomere sequence, do not terminate BIR at a significant frequency in wild-type cells. However, these sequences can form ectopic telomeres if BIR is made less processive. Our results support a model in which features of the ITS itself, such as the propensity to form secondary structures and telomeric protein binding, pose a challenge to BIR and increase the vulnerability of the D-loop to dissociation by helicases, thereby promoting ectopic telomere formation.

Indexed as

Recombination, GeneticDEAD-box RNA HelicasesDNA Breaks, Double-StrandedDNA DamageDNA HelicasesDNA Polymerase IIIDNA RepairDNA ReplicationSaccharomyces cerevisiaeSaccharomyces cerevisiae ProteinsTelomeraseTelomereDEAD-box RNA HelicasesDNA HelicasesDNA Polymerase IIIMPH1 protein, S cerevisiaeSaccharomyces cerevisiae ProteinsTelomerase

Identifiers

PMID33264397
PMCPMC7736798
OpenAlexW3108330114

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.