Evidence map›Paper›PMID 38710919›Full record

ArticleCellular and molecular life sciences : CMLS2024

PRDM14 extinction enables the initiation of trophoblast stem cell formation.

Chunfang Xu, Weijie Zhao, Lijin Peng, Tingxuan Yin, Jiani Guo, Yue Li, Lu Liu, Jinying Yang, Congjian Xu, Meirong Du

Abstract read
In one paragraph

Article in Cellular and molecular life sciences : CMLS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

10 authors.

Chunfang Xu *Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Weijie Zhao *Laboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Lijin PengLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Tingxuan YinLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Jiani GuoLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Yue LiDepartment of Obstetrics and Gynecology, Shanghai Fourth People's Hospital, School of Medicine, Tongji University Shanghai, Shanghai, 200434, China.
Lu LiuLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China.
Jinying YangLonggang District Maternity & Child Healthcare Hospital of Shenzhen City, Longgang Maternity Child Institute of Shantou University Medical College, Shenzhen, 518172, China.
Congjian XuLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China. xucongjian@gmail.com.
Meirong DuLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Hospital of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai, 200032, China. mrdu@fudan.edu.cn.ORCID http://orcid.org/0000-0002-5307-6784

Funding

MOST 2021YFE0206500NSFC 31970859NSFC 81630036NSFC 82271713NSFC U23A20405
6 · The paper itself

Abstract

Trophoblast stem cells (TSCs) can be chemically converted from embryonic stem cells (ESCs) in vitro. Although several transcription factors (TFs) have been recognized as essential for TSC formation, it remains unclear how differentiation cues link elimination of stemness with the establishment of TSC identity. Here, we show that PRDM14, a critical pluripotent circuitry component, is reduced during the formation of TSCs. The reduction is further shown to be due to the activation of Wnt/β-catenin signaling. The extinction of PRDM14 results in the erasure of H3K27me3 marks and chromatin opening in the gene loci of TSC TFs, including GATA3 and TFAP2C, which enables their expression and thus the initiation of the TSC formation process. Accordingly, PRDM14 reduction is proposed here as a critical event that couples elimination of stemness with the initiation of TSC formation. The present study provides novel insights into how induction signals initiate TSC formation.

Indexed as

Cell DifferentiationDNA-Binding ProteinsTranscription FactorsTrophoblastsWnt Signaling PathwayAnimalsGATA3 Transcription FactorHistonesMiceRNA-Binding ProteinsStem CellsTranscription Factor AP-2DNA-Binding ProteinsGATA3 Transcription FactorHistonesPrdm14 protein, mouseRNA-Binding ProteinsTfap2c protein, mouseTranscription Factor AP-2Transcription FactorsH3K27me3Human trophoblast stem cellsPRDM14Wnt

Identifiers

PMID38710919
PMCPMC11074026

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Registered trials

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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.