Evidence map›Paper›PMID 40097392›Full record

ArticleNature communications2025

A CPC-shelterin-BTR axis regulates mitotic telomere deprotection.

Diana Romero-Zamora, Samuel Rogers, Ronnie Ren Jie Low, Scott G Page, Blake J E Lane, Shunya Kosaka, Andrew B Robinson, Lucy French, Noa Lamm, Fuyuki Ishikawa and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
–field-weighted citation impact
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

7 citing papers in PubMed.

  1. Review
  2. Review
  3. Review
  4. Telomere Crisis Shapes Cancer Evolution.Cold Spring Harbor perspectives in biology · 2026
    Review
  5. iScience · 2026
    Article
  6. Article
  7. 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

12 authors.

Diana Romero-Zamora *Graduate School of Biostudies, Kyoto University, Sakyo, Kyoto, Japan.ORCID http://orcid.org/0009-0009-7078-5185
Samuel Rogers *Children's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.
Ronnie Ren Jie LowChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-2629-4778
Scott G PageChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0000-0002-4659-5543
Blake J E LaneChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.
Shunya KosakaGraduate School of Biostudies, Kyoto University, Sakyo, Kyoto, Japan.
Andrew B RobinsonChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.
Lucy FrenchChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.ORCID http://orcid.org/0009-0007-5568-6651
Noa LammChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia.
Fuyuki IshikawaGraduate School of Biostudies, Kyoto University, Sakyo, Kyoto, Japan.
Makoto T HayashiGraduate School of Biostudies, Kyoto University, Sakyo, Kyoto, Japan. makoto.hayashi@ifom.eu.
Anthony J CesareChildren's Medical Research Institute, University of Sydney, Sydney, NSW, Australia. tcesare@cmri.org.au.ORCID http://orcid.org/0000-0002-0864-1254

Funding

Department of Health | National Health and Medical Research Council (NHMRC) 1106241Department of Health | National Health and Medical Research Council (NHMRC) 1162886
6 · The paper itself

Abstract

Telomeres prevent ATM activation by sequestering chromosome termini within telomere loops (t-loops). Mitotic arrest promotes telomere linearity and a localized ATM-dependent telomere DNA damage response (DDR) through an unknown mechanism. Using unbiased interactomics, biochemical screening, molecular biology, and super-resolution imaging, we found that mitotic arrest-dependent (MAD) telomere deprotection requires the combined activities of the Chromosome passenger complex (CPC) on shelterin, and the BLM-TOP3A-RMI1/2 (BTR) complex on t-loops. During mitotic arrest, the CPC component Aurora Kinase B (AURKB) phosphorylated both the TRF1 hinge and TRF2 basic domains. Phosphorylation of the TRF1 hinge domain enhances CPC and TRF1 interaction through the CPC Survivin subunit. Meanwhile, phosphorylation of the TRF2 basic domain promotes telomere linearity, activates a telomere DDR dependent on BTR-mediated double Holliday junction dissolution, and leads to mitotic death. We identify that the TRF2 basic domain functions in mitosis-specific telomere protection and reveal a regulatory role for TRF1 in controlling a physiological ATM-dependent telomere DDR. The data demonstrate that MAD telomere deprotection is a sophisticated active mechanism that exposes telomere ends to signal mitotic stress.

Indexed as

Chromosomes, MammalianMitosisTelomereAnimalsCell DeathCells, CulturedDNA-Binding ProteinsDNA Topoisomerases, Type IFemaleHumansMaleMicePhosphorylationProtein BindingRecQ HelicasesSurvivinBIRC5 protein, humanBloom syndrome proteinDNA-Binding ProteinsDNA Topoisomerases, Type IRecQ HelicasesSurvivinTelomeric Repeat Binding Protein 1Telomeric Repeat Binding Protein 2

Identifiers

PMID40097392
PMCPMC11914695

What OpenQuestion holds

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LicenceCC BY
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.