Evidence map›Paper›PMID 42380617›Full record

ArticleNature structural & molecular biology2026

Distinct ATRX functions cooperate with 9-1-1 and CST complexes to safeguard replication and telomere integrity.

Sandra Segura-Bayona, Marija Maric, Tohru Takaki, Zornitsa Manova, Tyler H Stanage, Aurora I Idilli, Shudong Li, Graeme Hewitt, Feras E Machour, Rhona Millar and 10 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature structural & molecular biology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

20 authors.

Sandra Segura-BayonaDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0001-7788-9889
Marija MaricDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Tohru TakakiDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Zornitsa ManovaDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Tyler H StanageDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0003-1668-9909
Aurora I IdilliDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Shudong LiDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Graeme HewittDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Feras E MachourDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Rhona MillarDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Marek AdamowiczDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Ronnie Ren Jie LowDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-2629-4778
Phil RuisDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Benura AzerogluDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Todd FallesenCrick Advanced Light Microscopy STP, The Francis Crick Institute, London, UK.ORCID http://orcid.org/0000-0002-8700-3700
Harshil PatelBioinformatics and Biostatistics STP, The Francis Crick Institute, London, UK.
Steven HowellProteomics STP, The Francis Crick Institute, London, UK.
Panagiotis KotsantisDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK.
Michael HowellScreening and Automated Science STP, The Francis Crick Institute, London, UK.
Simon J BoultonDSB Repair Metabolism Laboratory, The Francis Crick Institute, London, UK. simon.boulton@crick.ac.uk.ORCID http://orcid.org/0000-0001-6936-6834

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the ATRX chromatin remodeler confer a predisposition to a developmental genetic disorder and cancer, but how ATRX safeguards genome and telomere stability remains unresolved. Here, we uncover critical dependencies for the CTC1-STN1-TEN1 (CST) complex and RAD9A-HUS1-RAD1 (9-1-1) clamp in ATRX-deficient cells. ATRX-CST synthetic lethality manifests following accumulation of telomeric G-rich single-stranded DNA (ssDNA), which results in telomere loss and cell death. Conversely, we attribute ATRX-9-1-1 synthetic lethality to genome-wide ssDNA lesions, which compromise DNA replication. We further show that ATRX suppresses DNA damage during replication stress by counteracting the activity of the FAM111A protease. We demonstrate that roles of ATRX in telomere maintenance and replication are genetically separable, requiring its ATPase activity and PIP-box, respectively. We also show that such roles protecting genome stability are largely independent of the ATRX-DAXX interaction. Collectively, our data show that functions of ATRX in suppressing toxic ssDNA lesions are context-dependent and are key to global DNA replication and telomere integrity.

Indexed as

Chromosomal Proteins, Non-HistoneDNA HelicasesDNA ReplicationNuclear ProteinsTelomereTelomere-Binding ProteinsCell Cycle ProteinsDNA DamageDNA, Single-StrandedGenomic InstabilityHumansX-linked Nuclear ProteinATRX protein, humanCell Cycle ProteinsChromosomal Proteins, Non-HistoneCtc1 protein, humanDNA HelicasesDNA, Single-StrandedNuclear ProteinsStn1 protein, humanTelomere-Binding ProteinsTen1 protein, humanX-linked Nuclear Protein

Identifiers

PMID42380617
PMCPMC13372662

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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.