Evidence map›Paper›PMID 40705605›Full record

ArticleCell reports2025

The mitotic ATR-Chk1 pathway promotes CDK1 activity for faithful chromosome segregation.

Yoon Ki Joo, Carlos Ramirez Parrado, Wenxue Li, Ran Yang, Elizabeth Black, Franziska Bleichert, Yansheng Liu, Lilian Kabeche

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing 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

5 citing papers in PubMed.

  1. Review
  2. Review
  3. Article
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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

8 authors.

Yoon Ki JooDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA; Yale Cancer Biology Institute, Yale University, West Haven, CT, USA.
Carlos Ramirez ParradoDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA; Yale Cancer Biology Institute, Yale University, West Haven, CT, USA.
Wenxue LiYale Cancer Biology Institute, Yale University, West Haven, CT, USA; Department of Pharmacology, Yale University, New Haven, CT, USA.
Ran YangDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.
Elizabeth BlackDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA; Yale Cancer Biology Institute, Yale University, West Haven, CT, USA.
Franziska BleichertDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA.
Yansheng LiuYale Cancer Biology Institute, Yale University, West Haven, CT, USA; Department of Pharmacology, Yale University, New Haven, CT, USA; Department of Biomedical Informatics & Data Science, Yale University, New Haven, CT, USA.
Lilian KabecheDepartment of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT, USA; Yale Cancer Biology Institute, Yale University, West Haven, CT, USA. Electronic address: lilian.kabeche@yale.edu.

Funding

Understanding proteome remodeling in aneuploidyR01GM137031 · NIGMS · YALE UNIVERSITY · PI LIU, YANSHENG · 2020 to 2024
$2.0M
Mechanisms for recruitment and function of metazoan replication initiation factorsR01GM141313 · NIGMS · YALE UNIVERSITY · PI BLEICHERT, FRANZISKA · 2021 to 2025
$1.7M
Elucidating how ATR promotes genome stability independent of the DNA damage response pathwayR35GM150648 · NIGMS · YALE UNIVERSITY · PI Lilian Carolina Kabeche · 2023 to 2026
$1.7M
NIGMS NIH HHS R01 GM137031NIGMS NIH HHS R01 GM141313NIGMS NIH HHS R35 GM150648
6 · The paper itself

Abstract

Ataxia telangiectasia and Rad3-related (ATR) and checkpoint kinase 1 (Chk1) are crucial kinases in the DNA damage response (DDR) pathway. While the roles of ATR and Chk1 within the DDR are well established, their roles in mitosis are not fully understood. Here, we describe that the ATR-Chk1 pathway is rewired during mitosis to promote full CDK1 activity, starkly contrasting its role in interphase, where it inhibits CDK1 following DNA damage in human cells. In mitosis, Chk1 inhibits residual activity of PKMYT1 (Myt1) via direct phosphorylation at Serine 143. Partial loss of CDK1 activity caused by inhibition of mitotic Chk1 leads to different effects on mitotic progression than full CDK1 inhibition. It causes increased lagging chromosomes in part through loss of Aurora B activity. Thus, mitosis-specific ATR-Chk1 activity is necessary to promote faithful chromosome segregation by ensuring that CDK1 activity is maintained in mitosis.

Indexed as

Ataxia Telangiectasia Mutated ProteinsCDC2 Protein KinaseCheckpoint Kinase 1Chromosome SegregationMitosisAurora Kinase BDNA DamageHeLa CellsHumansPhosphorylationSignal TransductionAtaxia Telangiectasia Mutated ProteinsATR protein, humanAURKB protein, humanAurora Kinase BCDC2 Protein KinaseCDK1 protein, humanCheckpoint Kinase 1CHEK1 protein, humanATRCDK1cell cycleChk1chromosome segregationCP: Molecular biologyDNA damage response pathwaymitosis

Identifiers

PMID40705605
PMCPMC12451630

What Socratic holds

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LicenceCC BY-NC
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Registered trials

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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 Socratic graph.