Evidence map›Paper›PMID 41654129›Full record

ArticleThe Journal of biological chemistry2026

Topologically associating domains define the 3D genome architecture of mouse totipotent-like stem cells.

Yu Fu, Wenyu Ma, Jin Han, Wenhui Zhang, Shenghu Zhang, Yuxiao Chen, Yue Qin, Junyang Li, Ziwei Zhai, Pengli Li and 11 more

Abstract read
In one paragraph

Article in The Journal of biological chemistry, 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

21 authors.

Yu FuSchool of Life Sciences, Fudan University, Shanghai, China; Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Wenyu MaLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Jin HanLife Sciences Institute and The Second Affiliated Hospital, Zhejiang University, Hangzhou, China.
Wenhui ZhangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Shenghu ZhangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Yuxiao ChenSchool of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Yue QinLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, China.
Junyang LiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; School of Life Sciences, Westlake University, Hangzhou, Zhejiang, China.
Ziwei ZhaiCentre for Regenerative Medicine and Health, Hong Kong Institute of Science & Innovation, Chinese Academy of Sciences, Hong Kong SAR, China.
Pengli LiCentre for Regenerative Medicine and Health, Hong Kong Institute of Science & Innovation, Chinese Academy of Sciences, Hong Kong SAR, China.
Wei LiLaboratory on Stem Cell and Regenerative Medicine, Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences, Guangzhou, China; Guangzhou Institutes of Biomedicine and Health, University of Chinese Academy of Sciences, Beijing, China.
Kaipeng WangSchool of Life Sciences, Fudan University, Shanghai, China; Laboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Zhaoyi MaLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Yuxiang YaoLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China.
Chengchen ZhaoLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, China.
Bo WangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; Zhejiang Key Laboratory of Biomedical Intelligent Computing Technology, Hangzhou, China; Zhejiang University of Science and Technology School of Information and Electronic Engineering, Hangzhou, China.
Haoxi ChaiLife Sciences Institute and The Second Affiliated Hospital, Zhejiang University, Hangzhou, China.
Yijun RuanLife Sciences Institute and The Second Affiliated Hospital, Zhejiang University, Hangzhou, China.
Junqi KuangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, China. Electronic address: kuangjunqi@westlake.edu.cn.
Zheting ZhangLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China. Electronic address: zhangzheting@westlake.edu.cn.
Duanqing PeiLaboratory of Cell Fate Control, School of Life Sciences, Westlake University, Hangzhou, China; Westlake Laboratory of Life Sciences and Biomedicine, Hangzhou, China. Electronic address: peiduanqing@westlake.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Totipotency is the first cell fate emerged from fertilization, but remains poorly understood at the molecular level. Totipotent blastomeres are characterized by the presence of topologically associating domains (TADs) with significantly weakened structural integrity. In this study, we performed high-resolution 3D genome architecture profiling of two established mouse totipotent-like models, chemically induced totipotent stem cells and totipotent blastomere-like cells, and revealed that both largely retained TADs found in inner cell mass /embryonic stem cells. Yet, amid the apparent TAD conservation, TAD strength was indeed considerably weakened upon the acquisition of totipotency. Integrative analysis of epigenetic and Hi-C data revealed that pluripotency genes underwent coordinated epigenetic landscape remodeling and 3D contact reorganization, which collectively drove pluripotency silencing. Epigenetic remodeling was also observed at totipotency gene loci. This work represents the first systematic effort to benchmark totipotency models at the 3D genome level and provides a framework to establish totipotency through 3D genome folding.

Indexed as

GenomeTotipotent Stem CellsAnimalsEpigenesis, GeneticMice3D genome organizationEpigeneticPluripotent stem cellsTotipotency-pluripotency transitionTotipotent stem cells

Identifiers

PMID41654129
PMCPMC12990084

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.