Evidence map›Paper›PMID 40296153›Full record

ArticleGenome biology2025

Rewiring of SINE-MIR enhancer topology and Esrrb modulation in expanded and naive pluripotency.

Nadia Omega Cipta, Yingying Zeng, Ka Wai Wong, Zi Hao Zheng, Yao Yi, Tushar Warrier, Jian Zhou Teo, Jia Hao Jackie Teo, Yee Jiun Kok, Xuezhi Bi and 7 more

Abstract read
In one paragraph

Article in Genome biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
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.

Nadia Omega Cipta *Epigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Yingying Zeng *Epigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Ka Wai WongEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Zi Hao ZhengEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Yao YiEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Tushar WarrierEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Jian Zhou TeoEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Jia Hao Jackie TeoEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore.
Yee Jiun KokProteomics Group, Agency for Science, Technology and Research (A*STAR), Bioprocessing Technology Institute (BTI), Singapore, 138668, Singapore.
Xuezhi BiProteomics Group, Agency for Science, Technology and Research (A*STAR), Bioprocessing Technology Institute (BTI), Singapore, 138668, Singapore.
Reshma TanejaDepartment of Physiology, NUS Yong Loo Lin School of Medicine, 2 Medical Drive, MD9, Singapore, Singapore.
Derrick Sek Tong OngDepartment of Physiology, NUS Yong Loo Lin School of Medicine, 2 Medical Drive, MD9, Singapore, Singapore.
Jian XuDepartment of Pathology, Center of Excellence for Leukemia Studies, St. Jude Children's Research Hospital, Memphis, TN, 38105, USA.
Florent GinhouxSingapore Immunology Network (SIgN), Agency for Science, Technology and Research (A*STAR), Singapore, Singapore.
Hu LiDepartment of Molecular Pharmacology & Experimental Therapeutics, Center for Individualized Medicine, Mayo Clinic, Rochester, MN, 55905, USA.
Yih-Cherng LiouDepartment of Biological Sciences, Faculty of Science, National University of Singapore, 14 Science Drive 4, Singapore, 117543, Singapore. dbslyc@nus.edu.sg.
Yuin-Han LohEpigenetics and Cell Fates Laboratory, Cell Fate Engineering and Therapeutics Laboratory, Institute of Molecular and Cell Biology (IMCB), Agency for Science, Technology and Research (A*STAR), 61 Biopolis Drive Proteos, Singapore, 138673, Singapore. yhloh@imcb.a-star.edu.sg.

Funding

TRAININGU54GM114838 · NIGMS · UNIVERSITY OF ILLINOIS AT URBANA-CHAMPAIGN · PI HAN, JIAWEI, SINHA, SAURABH · 2014 to 2017
$10.8M
A network platform to connect drug response and prognosis phenotypes for cancersR01CA196631 · NCI · MAYO CLINIC ROCHESTER · PI LI, HU · 2016 to 2018
$1.2M
A*STAR C211318012A*STAR W22W3D0007IAF-PP H1801a0021National Institute of Health CA196631-01A1National Medical Research Council OFIRG21nov-0088NCI NIH HHS R01 CA196631NIGMS NIH HHS 1U54GM114838-01NIGMS NIH HHS U54 GM114838NRF NRF2019-THE002-0001NRF Investigatorship Award NRFI2018-02
6 · The paper itself

Abstract

backgroundThe interplay between 3D genomic structure and transposable elements (TE) in regulating cell state-specific gene expression program is largely unknown. Here, we explore the utilization of TE-derived enhancers in naïve and expanded pluripotent states by integrative analysis of genome-wide Hi-C-defined enhancer interactions, H3K27ac HiChIP profiling and CRISPR-guided TE proteomics landscape.

resultsWe find that short interspersed nuclear elements (SINEs) are the more involved TEs in the active chromatin and 3D genome architecture. In particular, mammalian-wide interspersed repeat (MIR), a SINE family member, is highly associated with naïve-specific genomic interactions compared to the expanded state. Primarily, in the naïve pluripotent state, MIR enhancer is co-opted by ESRRB for naïve-specific gene expression program. This ESRRB and MIR enhancer interaction is crucial for the formation of loops that build a network of enhancers and super-enhancers regulating pluripotency genes. We demonstrate that loss of a ESRRB-bound MIR enhancer impairs self-renewal. We also find that MIR is co-bound by structural protein complex, ESRRB-YY1, in the naïve pluripotent state.

conclusionsAltogether, our study highlights the topological regulation of ESRRB on MIR in the naïve potency state.

Indexed as

Enhancer Elements, GeneticMicroRNAsPluripotent Stem CellsShort Interspersed Nucleotide ElementsAnimalsHumansMiceReceptors, EstrogenEsrrb protein, mouseMicroRNAsReceptors, Estrogen3D genomeMouse embryonic stem cellsPluripotencyTransposable element

Identifiers

PMID40296153
PMCPMC12036290

What OpenQuestion holds

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LicenceCC BY-NC-ND
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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.