Evidence map›Paper›PMID 18502190›Full record

ArticleDNA repair2008

Telomerase-dependent and -independent chromosome healing in mouse embryonic stem cells.

Qing Gao, Gloria E Reynolds, Andrew Wilcox, Douglas Miller, Peggie Cheung, Steven E Artandi, John P Murnane

Open access · greenAbstract read
In one paragraph

Article in DNA repair, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Article
  2. Centromere scission drives chromosome shuffling and reproductive isolation.Proceedings of the National Academy of Sciences of the United States of America · 2020
    Article
  3. Article
  4. Article
  5. Article
  6. Article
  7. Telomeres and genomic evolution.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2018
    Review
  8. Article
  9. Article
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  11. Article
  12. Review
  13. Article
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  15. Article
  16. Review
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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 1 country.

Qing GaoDepartment of Radiation Oncology, University of California, San Francisco, CA 94103, USA.
Gloria E Reynolds
Andrew Wilcox
Douglas Miller
Peggie Cheung
Steven E Artandi
John P Murnane
University of California, San Francisco · USStanford Medicine · US

Funding

MECHANISMS OF FORMATION OF TERMINAL DELETIONSR01ES008427 · NIEHS · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI MURNANE, JOHN P. · 1997 to 2007
$2.5M
NIEHS NIH HHS R01 ES 008427NIEHS NIH HHS R01 ES008427
6 · The paper itself

Abstract

Telomeres play an important role in protecting the ends of chromosomes and preventing chromosome fusion. We have previously demonstrated that double-strand breaks near telomeres in mammalian cells result in either the addition of a new telomere at the site of the break, termed chromosome healing, or sister chromatid fusion that initiates chromosome instability. In the present study, we have investigated the role of telomerase in chromosome healing and the importance of chromosome healing in preventing chromosome instability. In embryonic stem cell lines that are wild type for the catalytic subunit of telomerase (TERT), chromosome healing at I-SceI-induced double-strand breaks near telomeres accounted for 22 of 35 rearrangements, with the new telomeres added directly at the site of the break in all but one instance. In contrast, in two TERT-knockout embryonic stem cell lines, chromosome healing accounted for only 1 of 62 rearrangements, with a 23 bp insertion at the site of the sole chromosome-healing event. However, in a third TERT-knockout embryonic stem cell line, 10PTKO-A, chromosome healing was a common event that accounted for 20 of 34 rearrangements. Although this chromosome healing also occurred at the I-SceI site, differences in the microhomology at the site of telomere addition demonstrated that the mechanism was distinct from that in wild-type embryonic stem cell lines. In addition, the newly added telomeres in 10PTKO-A shortened with time in culture, eventually resulting in either telomere elongation through a telomerase-independent mechanism or loss of the subtelomeric plasmid sequences entirely. The combined results demonstrate that chromosome healing can occur through both telomerase-dependent and -independent mechanisms, and that although both mechanisms can prevent degradation and sister chromatid fusion, neither mechanism is efficient enough to prevent sister chromatid fusion from occurring in many cells experiencing double-strand breaks near telomeres.

Indexed as

ChromosomesAnimalsBase SequenceDNA PrimersEmbryonic Stem CellsMiceMice, KnockoutMice, TransgenicMolecular Sequence DataSequence Homology, Nucleic AcidTelomeraseDNA PrimersTelomeraseTert protein, mouse

Identifiers

PMID18502190
PMCPMC2597172
OpenAlexW2049240112

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.