Evidence map›Paper›PMID 37591949›Full record

ArticleNature cell biology2023

Young LINE-1 transposon 5' UTRs marked by elongation factor ELL3 function as enhancers to regulate naïve pluripotency in embryonic stem cells.

Siyan Meng, Xiaoxu Liu, Shiqi Zhu, Peng Xie, Haitong Fang, Qingyun Pan, Ke Fang, Fanfan Li, Jin Zhang, Zhuanzhuan Che and 9 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature cell biology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
13.1field-weighted citation impact, top 1% of its field
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

22 citing papers in PubMed, 33 citations in OpenAlex.

  1. SEC Mediates mAdvanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
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  17. TET activity safeguards pluripotency throughout embryonic dormancy.Nature structural & molecular biology · 2024
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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

19 authors at 4 institutions in 2 countries.

Siyan Meng *Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Xiaoxu Liu *Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Shiqi Zhu *Key Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Peng Xie *School of Biological Science and Medical Engineering, Southeast University, Nanjing, China.ORCID http://orcid.org/0000-0002-9509-7268
Haitong FangKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Qingyun PanKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Ke FangKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Fanfan LiKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Jin ZhangKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Zhuanzhuan CheKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Quanyong ZhangState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, China.
Guangyao MaoKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Yan WangDepartment of Prenatal Diagnosis, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, China.
Ping HuDepartment of Prenatal Diagnosis, Women's Hospital of Nanjing Medical University, Nanjing Maternity and Child Health Care Hospital, Nanjing, China.
Kai ChenState Key Laboratory of Primate Biomedical Research, Institute of Primate Translational Medicine, Kunming University of Science and Technology, Kunming, China.
Fei SunKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.
Wei XieKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China.ORCID http://orcid.org/0000-0002-9179-4787
Zhuojuan LuoKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China. zjluo@seu.edu.cn.ORCID http://orcid.org/0000-0002-0715-0648
Chengqi LinKey Laboratory of Developmental Genes and Human Disease, School of Life Science and Technology, Southeast University, Nanjing, China. cqlin@seu.edu.cn.ORCID http://orcid.org/0000-0002-2121-584X
Southeast University · CNNantong University · CNKunming University of Science and Technology · CNNanjing Maternity and Child Health Care Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

LINE-1s are the major clade of retrotransposons with autonomous retrotransposition activity. Despite the potential genotoxicity, LINE-1s are highly activated in early embryos. Here we show that a subset of young LINE-1s, L1Md_Ts, are marked by the RNA polymerase II elongation factor ELL3, and function as enhancers in mouse embryonic stem cells. ELL3 depletion dislodges the DNA hydroxymethylase TET1 and the co-repressor SIN3A from L1Md_Ts, but increases the enrichment of the Bromodomain protein BRD4, leading to loss of 5hmC, gain of H3K27ac, and upregulation of the L1Md_T nearby genes. Specifically, ELL3 occupies and represses the L1Md_T-based enhancer located within Akt3, which encodes a key regulator of AKT pathway. ELL3 is required for proper ERK activation and efficient shutdown of naïve pluripotency through inhibiting Akt3 during naïve-primed transition. Our study reveals that the enhancer function of a subset of young LINE-1s controlled by ELL3 in transcription regulation and mouse early embryo development.

Indexed as

Nuclear ProteinsTranscription Factors5' Untranslated RegionsAnimalsEmbryonic Stem CellsMicePeptide Elongation Factors5' Untranslated RegionsNuclear ProteinsPeptide Elongation FactorsTranscription Factors

Identifiers

PMID37591949
OpenAlexW4385948560

What OpenQuestion holds

Textmetadata
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.