Evidence map›Paper›PMID 32960220›Full record

ArticleNucleic acids research2020

Embryonic erythropoiesis and hemoglobin switching require transcriptional repressor ETO2 to modulate chromatin organization.

Xiang Guo, Jennifer Plank-Bazinet, Ivan Krivega, Ryan K Dale, Ann Dean

Open access · goldAbstract read
In one paragraph

Article in Nucleic acids research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

23 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. New Gene Therapy Strategy for β-Thalassemia.Stem cell reviews and reports · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Article
  10. Article
  11. Article
  12. MYB represses ζ-globin expression through upregulating ETO2.Acta biochimica et biophysica Sinica · 2025
    Article
  13. LDB1 establishes multi-enhancer networks to regulate gene expression.bioRxiv : the preprint server for biology · 2024
    Article
  14. Article
  15. Article
  16. Article
  17. Review
  18. Article
  19. Review
  20. 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

5 authors at 1 institution in 1 country.

Xiang GuoLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Building 50, Room 3154, Bethesda, MD 20892, USA.
Jennifer Plank-BazinetLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Building 50, Room 3154, Bethesda, MD 20892, USA.
Ivan KrivegaLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Building 50, Room 3154, Bethesda, MD 20892, USA.
Ryan K DaleLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Building 50, Room 3154, Bethesda, MD 20892, USA.
Ann DeanLaboratory of Cellular and Developmental Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, 50 South Drive, Building 50, Room 3154, Bethesda, MD 20892, USA.
National Institutes of Health · US

Funding

Epigenetic and Developmental Regulation of Mammalian GenesZIADK075033 · NIDDK · NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES · PI DEAN, ANN · 2009 to 2025
$24.2M
Intramural NIH HHS ZIA DK075033
6 · The paper itself

Abstract

The underlying mechanism of transcriptional co-repressor ETO2 during early erythropoiesis and hemoglobin switching is unclear. We find that absence of ETO2 in mice interferes with down-regulation of PU.1 and GATA2 in the fetal liver, impeding a key step required for commitment to erythroid maturation. In human β-globin transgenic Eto2 null mice and in human CD34+ erythroid progenitor cells with reduced ETO2, loss of ETO2 results in ineffective silencing of embryonic/fetal globin gene expression, impeding hemoglobin switching during erythroid differentiation. ETO2 occupancy genome-wide occurs virtually exclusively at LDB1-complex binding sites in enhancers and ETO2 loss leads to increased enhancer activity and expression of target genes. ETO2 recruits the NuRD nucleosome remodeling and deacetylation complex to regulate histone acetylation and nucleosome occupancy in the β-globin locus control region and γ-globin gene. Loss of ETO2 elevates LDB1, MED1 and Pol II in the locus and facilitates fetal γ-globin/LCR looping and γ-globin transcription. Absence of the ETO2 hydrophobic heptad repeat region impairs ETO2-NuRD interaction and function in antagonizing γ-globin/LCR looping. Our results reveal a pivotal role for ETO2 in erythropoiesis and globin gene switching through its repressive role in the LDB1 complex, affecting the transcription factor and epigenetic environment and ultimately restructuring chromatin organization.

Indexed as

ErythropoiesisAnimalsChromatinChromatin Assembly and DisassemblyDNA-Binding ProteinsErythroid Cellsgamma-GlobinsHumansK562 CellsLIM Domain ProteinsMi-2 Nucleosome Remodeling and Deacetylase ComplexMiceMice, KnockoutRepressor ProteinsTranscription FactorsCBFA2T3 protein, humanChromatinDNA-Binding Proteinsgamma-GlobinsLDB1 protein, humanLIM Domain ProteinsMi-2 Nucleosome Remodeling and Deacetylase ComplexRepressor ProteinsTranscription Factors

Identifiers

PMID32960220
PMCPMC7544236
OpenAlexW3087617216

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.