Evidence map›Paper›PMID 32240602›Full record

ArticleMolecular cell2020

Cdk1 Controls Global Epigenetic Landscape in Embryonic Stem Cells.

Wojciech Michowski, Joel M Chick, Chen Chu, Aleksandra Kolodziejczyk, Yichen Wang, Jan M Suski, Brian Abraham, Lars Anders, Daniel Day, Lukas M Dunkl and 19 more

Abstract read
In one paragraph

Article in Molecular cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.

0numbers the graph read from it
0cells of the map it votes in
72citing 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

72 citing papers in PubMed.

  1. Article
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  6. Decoding Cdk1 control: from mitotic thresholds to meiotic specificity.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2026
    Review
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  15. Article
  16. CDK1-loaded extracellular vesicles promote cell cycle to reverse impaired wound healing in diabetic obese mice.Molecular therapy : the journal of the American Society of Gene Therapy · 2025
    Article
  17. Article
  18. Article
  19. Article
  20. Article

12 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

29 authors.

Wojciech MichowskiDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA; Department of Oncologic Pathology, Dana-Farber Cancer Institute, Boston, MA 02215, USA.
Joel M ChickDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Chen ChuDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Aleksandra KolodziejczykDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Yichen WangSchool of Life Sciences, Peking University, Beijing 100871, China.
Jan M SuskiDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Brian AbrahamWhitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Lars AndersWhitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Daniel DayWhitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Lukas M DunklDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Mitchell Li Cheong ManDepartment of Cell and Systems Biology, University of Toronto, Toronto, ON M5S 3B2, Canada.
Tian ZhangDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Phatthamon LaphanuwatDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Nickolas A BaconDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Lijun LiuDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Anne FasslDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Samanta SharmaDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Tobias OttoDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Emanuelle JecroisDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Richard HanDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Katharine E SweeneyDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Samuele MarroInstitute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University Medical School, Stanford, CA 94305, USA.
Marius WernigInstitute for Stem Cell Biology and Regenerative Medicine and Department of Pathology, Stanford University Medical School, Stanford, CA 94305, USA.
Yan GengDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA.
Alan MosesDepartment of Cell and Systems Biology, University of Toronto, Toronto, ON M5S 3B2, Canada; Center for Analysis of Genome Evolution and Function, Toronto, ON M5S 3B2, Canada.
Cheng LiSchool of Life Sciences, Peking University, Beijing 100871, China.
Steven P GygiDepartment of Cell Biology, Harvard Medical School, Boston, MA 02115, USA.
Richard A YoungWhitehead Institute for Biomedical Research, Cambridge, MA 02142, USA; Department of Biology, Massachusetts Institute of Technology, Cambridge, MA 02142, USA.
Piotr SicinskiDepartment of Cancer Biology, Dana-Farber Cancer Institute, Boston, MA 02215, USA; Department of Genetics, Blavatnik Institute, Harvard Medical School, Boston, MA 02115, USA. Electronic address: peter_sicinski@dfci.harvard.edu.

Funding

Cyclin A Function in Stem Cells and in NeoplasiaR01CA132740 · NCI · DANA-FARBER CANCER INST · PI SICINSKI, PETER · 2008 to 2017
$4.4M
Transcriptional regulatory networks in living cellsR01GM123511 · NIGMS · WHITEHEAD INSTITUTE FOR BIOMEDICAL RES · PI YOUNG, RICHARD · 2017 to 2020
$3.6M
The function of cyclin C in tumorigenesisR01CA190509 · NCI · DANA-FARBER CANCER INST · PI SICINSKI, PETER · 2015 to 2019
$2.3M
Novel functions of D-type and E-type cyclins in normal and in cancer cellsR01CA202634 · NCI · DANA-FARBER CANCER INST · PI SICINSKI, PETER · 2016 to 2020
$2.1M
Functions of Cyclin/CDK complexes in development and cancerR50CA243769 · NCI · DANA-FARBER CANCER INST · PI GENG, YAN · 2019 to 2023
$898k
NCI NIH HHS R01 CA132740NCI NIH HHS R01 CA190509NCI NIH HHS R01 CA202634NCI NIH HHS R50 CA243769NIGMS NIH HHS R01 GM123511
6 · The paper itself

Abstract

The cyclin-dependent kinase 1 (Cdk1) drives cell division. To uncover additional functions of Cdk1, we generated knockin mice expressing an analog-sensitive version of Cdk1 in place of wild-type Cdk1. In our study, we focused on embryonic stem cells (ESCs), because this cell type displays particularly high Cdk1 activity. We found that in ESCs, a large fraction of Cdk1 substrates is localized on chromatin. Cdk1 phosphorylates many proteins involved in epigenetic regulation, including writers and erasers of all major histone marks. Consistent with these findings, inhibition of Cdk1 altered histone-modification status of ESCs. High levels of Cdk1 in ESCs phosphorylate and partially inactivate Dot1l, the H3K79 methyltransferase responsible for placing activating marks on gene bodies. Decrease of Cdk1 activity during ESC differentiation de-represses Dot1l, thereby allowing coordinated expression of differentiation genes. These analyses indicate that Cdk1 functions to maintain the epigenetic identity of ESCs.

Indexed as

Epigenesis, GeneticAdenosine TriphosphateAnimalsCDC2 Protein KinaseCell DifferentiationCells, CulturedChromatin ImmunoprecipitationEmbryonic Stem CellsFemaleHistone-Lysine N-MethyltransferaseHumansMaleMCF-7 CellsMiceMice, KnockoutPhosphorylationadenosine 5'-O-(3-thiotriphosphate)Adenosine TriphosphateCDC2 Protein KinaseCdk1 protein, mouseDot1l protein, mouseHistone-Lysine N-MethyltransferaseSaccharomyces cerevisiae Proteinsanalog sensitive kinasecell cyclecyclincyclin dependent kinasedifferentiationembryonic stem cellsepigeneticsphosphoproteomics

Identifiers

PMID32240602
PMCPMC7214218

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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.