Evidence map›Paper›PMID 39557885›Full record

ArticleScientific reports2024

Cooperative role of LSD1 and CHD7 in regulating differentiation of mouse embryonic stem cells.

Sandhya Malla, Carlos Martinez-Gamero, Kanchan Kumari, Cyrinne Achour, Georgios Mermelekas, David Martinez-Delgado, Alba Coego, Diana Guallar, Angel-Carlos Roman, Francesca Aguilo

Abstract read
In one paragraph

Article in Scientific reports, 2024. 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. [Kallmann syndrome in a girl caused by a novelZhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2026
    Article
  2. Article
  3. 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

10 authors.

Sandhya MallaDepartment of Molecular Biology, Umeå University, 901 85, Umeå, Sweden.
Carlos Martinez-GameroDepartment of Molecular Biology, Umeå University, 901 85, Umeå, Sweden.
Kanchan KumariDepartment of Molecular Biology, Umeå University, 901 85, Umeå, Sweden.
Cyrinne AchourDepartment of Molecular Biology, Umeå University, 901 85, Umeå, Sweden.
Georgios MermelekasScience for Life Laboratory, Department of Oncology-Pathology, Karolinska Institutet, 171 21, Solna, Sweden.
David Martinez-DelgadoCenter for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela (USC)-Health Research Institute (IDIS), Santiago de Compostela, Spain.
Alba CoegoCenter for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela (USC)-Health Research Institute (IDIS), Santiago de Compostela, Spain.
Diana GuallarCenter for Research in Molecular Medicine and Chronic Diseases (CIMUS), Universidade de Santiago de Compostela (USC)-Health Research Institute (IDIS), Santiago de Compostela, Spain.
Angel-Carlos RomanDepartment of Biochemistry, Molecular Biology and Genetics, University of Extremadura, Badajoz, Spain.
Francesca AguiloDepartment of Molecular Biology, Umeå University, 901 85, Umeå, Sweden. francesca.aguilo@umu.se.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Lysine-specific histone demethylase 1 (LSD1) is a histone demethylase that plays a critical role in epigenetic regulation by removing the methyl group from mono- and di-methylated lysine 4 on histone H3 (H3K4me1/2), acting as a repressor of gene expression. Recently, catalytically independent functions of LSD1, serving as a scaffold for assembling chromatin-regulator and transcription factor complexes, have been identified. Herein, we show for the first time that LSD1 interacts with chromodomain-helicase-DNA-binding protein 7 (CHD7) in mouse embryonic stem cells (ESCs). To further investigate the CHD7-LSD1 crosstalk, we engineered Chd7 and Chd7/Lsd1 knockout (KO) mouse ESCs. We show that CHD7 is dispensable for ESC self-renewal and survival, while Chd7 KO ESCs can differentiate towards embryoid bodies (EBs) with defective expression of ectodermal markers. Intriguingly, Chd7/Lsd1 double KO mouse ESCs exhibit proliferation defects similar to Lsd1 KO ESCs and have lost the capacity to differentiate properly. Furthermore, the increased co-occupancy of H3K4me1 and CHD7 on chromatin following Lsd1 deletion suggests that LSD1 is required for facilitating the proper binding of CHD7 to chromatin and regulating differentiation. Collectively, our results suggest that LSD1 and CHD7 work in concert to modulate gene expression and influence proper cell fate determination.

Indexed as

Cell DifferentiationDNA-Binding ProteinsHistone DemethylasesMice, KnockoutMouse Embryonic Stem CellsAnimalsCell ProliferationHistonesMiceProtein BindingChd7 protein, mouseDNA-Binding ProteinsHistone DemethylasesHistonesKDM1a protein, mouse

Identifiers

PMID39557885
PMCPMC11574112

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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.