Evidence map›Paper›PMID 41565645›Full record

ArticleNature communications2026

WDR5 remodels NANOG condensates to drive transcriptional programs and sustain stem cell identity.

Duo Wang, Xianle Shi, Jiaying Xie, Lijie Zhao, Bin Wu, Qiman Dong, Yaoguang Huang, Jinlong Suo, Xinyu Wang, Beixuan He and 7 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Review
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

17 authors.

Duo Wang *State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Xianle Shi *Department of Medicine, Columbia Center for Human Development and Stem Cell Therapies, Columbia University Irving Medical Center, New York, NY, USA.
Jiaying Xie *State Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Lijie Zhao *Key Laboratory of Epigenetic Regulation and Intervention, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.ORCID 0000-0002-0490-0175
Bin Wu *Protein Data Bank China (PDBc), Shanghai Advanced Research Institute, CAS, Shanghai, China.ORCID 0000-0003-4955-2765
Qiman DongDepartment of Thyroid and Neck Cancer, Tianjin Medical University Cancer Institute and Hospital, National Clinical Research Center for Cancer, Key Laboratory of Cancer Prevention and Therapy, Tianjin's Clinical Research Center for Cancer, Tianjin, China.
Yaoguang HuangKey Laboratory of Epigenetic Regulation and Intervention, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
Jinlong SuoInstitute of Microsurgery on Extremities, Department of Orthopedic Surgery, Shanghai Sixth People's Hospital Affiliated with Shanghai Jiao Tong University School of Medicine, Shanghai, China.ORCID 0000-0003-3389-3776
Xinyu WangState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Beixuan HeState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China.
Shukun YanKey Laboratory of Epigenetic Regulation and Intervention, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China.
Hongjuan XueNational Facility for Protein Science in Shanghai, Zhangjiang Lab, Shanghai Advanced Research Institute, Chinese Academy of Science, Shanghai, China.
Yuheng ShiCenter of Precision Medicine for Blood Diseases, Huashan Hospital, Zhongshan-Xuhui Hospital, Shanghai Key Laboratory of Medical Epigenetics, Institutes of Biomedical Sciences, Medical College of Fudan University, Shanghai, China.ORCID 0009-0002-6999-5600
Yingbin LiuState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. laoniulyb@shsmu.edu.cn.ORCID 0000-0001-6110-0185
Jianlong WangDepartment of Medicine, Columbia Center for Human Development and Stem Cell Therapies, Columbia University Irving Medical Center, New York, NY, USA. jw3925@cumc.columbia.edu.ORCID 0000-0002-1317-6457
Yong ChenKey Laboratory of Epigenetic Regulation and Intervention, Shanghai Institute of Biochemistry and Cell Biology, Center for Excellence in Molecular Cell Science, Chinese Academy of Sciences; University of Chinese Academy of Sciences, Shanghai, China. yongchen@sibcb.ac.cn.ORCID 0000-0001-5857-6086
Yanjing LiState Key Laboratory of Systems Medicine for Cancer, Shanghai Cancer Institute, Renji Hospital Affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, China. liyanjing@sjtu.edu.cn.ORCID 0000-0002-0747-6947

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32471528, 32071195, 32300480, 82400135
6 · The paper itself

Abstract

Stem cell pluripotency relies on a finely tuned interplay between transcription factors and epigenetic regulators. Here, we identify a direct interaction between NANOG, a master pluripotency transcription factor, and WDR5, a core chromatin regulator essential for maintaining stem cell identity. Mechanistically, WDR5 remodels irregular NANOG aggregates into dynamic, liquid-liquid phase-separated condensates at pluripotency-associated promoters to activate target genes. Structural analyses show that the NANOG homeodomain engages WDR5 through an extended interface distinct from previously characterized short linear motifs. The NANOG R153A mutation disrupts this interaction, leading to impaired condensate formation, reduced chromatin co-occupancy, and diminished levels of active histone marks, ultimately compromising embryonic stem cell pluripotency. Pharmacological inhibition of the WDR5-NANOG interaction suppresses leukemia stem cell expansion in vivo, highlighting its therapeutic potential. Collectively, this study reveals that WDR5-dependent regulation of NANOG condensate dynamics links phase-separated assemblies to transcriptional control of stem cell identity in physiological and pathological contexts.

Indexed as

Intracellular Signaling Peptides and ProteinsNanog Homeobox ProteinPluripotent Stem CellsAnimalsChromatinEmbryonic Stem CellsHumansMicePromoter Regions, GeneticTranscription, GeneticChromatinIntracellular Signaling Peptides and ProteinsNanog Homeobox ProteinNANOG protein, humanNanog protein, mouseWDR5 protein, humanWdr5 protein, mouse

Identifiers

PMID41565645
PMCPMC12923824

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.