Evidence map›Paper›PMID 33851958›Full record

ArticleThe Journal of cell biology2021

Telomere erosion in human pluripotent stem cells leads to ATR-mediated mitotic catastrophe.

Alexandre T Vessoni, Tianpeng Zhang, Annabel Quinet, Ho-Chang Jeong, Michael Munroe, Matthew Wood, Enzo Tedone, Alessandro Vindigni, Jerry W Shay, Roger A Greenberg and 1 more

Open access · greenAbstract read
In one paragraph

Article in The Journal of cell biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

9 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Review
  6. Compromised Mitotic Fidelity in Human Pluripotent Stem Cells.International journal of molecular sciences · 2023
    Review
  7. Article
  8. Review
  9. 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

11 authors at 3 institutions in 1 country.

Alexandre T VessoniDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Tianpeng ZhangDepartment of Cancer Biology, Penn Center for Genome Integrity, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Annabel QuinetDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Ho-Chang JeongDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Michael MunroeDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Matthew WoodDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Enzo TedoneDepartment of Cell Biology, UT Southwestern Medical Center, Dallas, TX.
Alessandro VindigniDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Jerry W ShayDepartment of Cell Biology, UT Southwestern Medical Center, Dallas, TX.
Roger A GreenbergDepartment of Cancer Biology, Penn Center for Genome Integrity, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Luis F Z BatistaDepartment of Medicine, Washington University in St. Louis, St. Louis, MO.
Washington University in St. Louis · USSouthwestern Medical Center · USUniversity of Pennsylvania · US

Funding

Washington University Center for Cellular ImagingP30CA091842 · NCI · WASHINGTON UNIVERSITY · PI TIMOTHY J. EBERLEIN · 2001 to 2026
$128.0M
PRE-AND POSTGRADUATE TRAINING IN MOLECULAR HEMATOLOGYT32HL007088 · NHLBI · WASHINGTON UNIVERSITY · PI Grant Anthony Challen, Stephen Oh · 1985 to 2026
$14.1M
Roles of Chromatin Modification in BRCA1 Dependent DNA RepairR01CA174904 · NCI · UNIVERSITY OF PENNSYLVANIA · PI Roger A Greenberg · 2013 to 2026
$4.8M
DNA Double Strand Break Chromatin Alterations and Genome IntegrityR01GM101149 · NIGMS · UNIVERSITY OF PENNSYLVANIA · PI GREENBERG, ROGER A · 2013 to 2025
$4.0M
Replication fork repriming versus reversalR01CA237263 · NCI · WASHINGTON UNIVERSITY · PI Alessandro Vindigni · 2019 to 2026
$3.0M
MOLECULAR CONSEQUENCES OF TELOMERASE DYSFUNCTION DURING HEMATOPOIETIC DEVELOPMENTR01HL137793 · NHLBI · WASHINGTON UNIVERSITY · PI BATISTA, LUIS FRANCISCO ZIRNBERGER · 2017 to 2021
$1.9M
NCI NIH HHS P30 CA091842NCI NIH HHS R01 CA174904NCI NIH HHS R01 CA237263NHLBI NIH HHS R01 HL137793NHLBI NIH HHS T32 HL007088NIGMS NIH HHS R01 GM101149
6 · The paper itself

Abstract

It is well established that short telomeres activate an ATM-driven DNA damage response that leads to senescence in terminally differentiated cells. However, technical limitations have hampered our understanding of how telomere shortening is signaled in human stem cells. Here, we show that telomere attrition induces ssDNA accumulation (G-strand) at telomeres in human pluripotent stem cells (hPSCs), but not in their differentiated progeny. This led to a unique role for ATR in the response of hPSCs to telomere shortening that culminated in an extended S/G2 cell cycle phase and a longer period of mitosis, which was associated with aneuploidy and mitotic catastrophe. Loss of p53 increased resistance to death, at the expense of increased mitotic abnormalities in hPSCs. Taken together, our data reveal an unexpected dominant role of ATR in hPSCs, combined with unique cell cycle abnormalities and, ultimately, consequences distinct from those observed in their isogenic differentiated counterparts.

Indexed as

Cell CycleMitosisAneuploidyAtaxia Telangiectasia Mutated ProteinsCell Cycle ProteinsDNA DamageHumansPluripotent Stem CellsTelomereTumor Suppressor Protein p53Ataxia Telangiectasia Mutated ProteinsATR protein, humanCell Cycle ProteinsTP53 protein, humanTumor Suppressor Protein p53

Identifiers

PMID33851958
PMCPMC8050844
OpenAlexW3153338733

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.