Evidence map›Paper›PMID 32391789›Full record

ArticleeLife2020

Linker histone H1.2 and H1.4 affect the neutrophil lineage determination.

Gabriel Sollberger, Robert Streeck, Falko Apel, Brian Edward Caffrey, Arthur I Skoultchi, Arturo Zychlinsky

Open access · goldAbstract read
In one paragraph

Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.0field-weighted citation impact, top 26% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. iScience · 2026
    Article
  2. Article
  3. Linker histone regulates the myeloid versus lymphoid bifurcation of multipotent hematopoietic stem and progenitors.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  4. Article
  5. M2 Macrophage-Derived Extracellular Vesicles Reprogram Immature Neutrophils into Anxa1Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Hinfp is a guardian of the somatic genome by repressing transposable elements.Proceedings of the National Academy of Sciences of the United States of America · 2021
    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

6 authors at 5 institutions in 3 countries.

Gabriel SollbergerMax Planck Institute for Infection Biology, Department of Cellular Microbiology, Berlin, Germany.ORCID 0000-0003-3647-9714
Robert StreeckMax Planck Institute for Infection Biology, Department of Cellular Microbiology, Berlin, Germany.
Falko ApelMax Planck Institute for Infection Biology, Department of Cellular Microbiology, Berlin, Germany.
Brian Edward CaffreyMax Planck Institute for Molecular Genetics, Berlin, Germany.
Arthur I SkoultchiDepartment of Cell Biology, Albert Einstein College of Medicine, Bronx, United States.
Arturo ZychlinskyMax Planck Institute for Infection Biology, Department of Cellular Microbiology, Berlin, Germany.
Humboldt-Universität zu Berlin · DEAlbert Einstein College of Medicine · USBerlin Institute of Health at Charité - Universitätsmedizin Berlin · DEMax Planck Institute for Infection Biology · DEUniversity of Dundee · GB

Funding

Functions of Mammalian H1 Linker Histones in Gene Regulation and DevelopmentR01GM116143 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI SKOULTCHI, ARTHUR I · 2015 to 2018
$1.9M
NIGMS NIH HHS GM116143NIGMS NIH HHS R01 GM116143Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung P2EZP3_148748Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung P300P3_158518
6 · The paper itself

Abstract

Neutrophils are important innate immune cells that tackle invading pathogens with different effector mechanisms. They acquire this antimicrobial potential during their maturation in the bone marrow, where they differentiate from hematopoietic stem cells in a process called granulopoiesis. Mature neutrophils are terminally differentiated and short-lived with a high turnover rate. Here, we show a critical role for linker histone H1 on the differentiation and function of neutrophils using a genome-wide CRISPR/Cas9 screen in the human cell line PLB-985. We systematically disrupted expression of somatic H1 subtypes to show that individual H1 subtypes affect PLB-985 maturation in opposite ways. Loss of H1.2 and H1.4 induced an eosinophil-like transcriptional program, thereby negatively regulating the differentiation into the neutrophil lineage. Importantly, H1 subtypes also affect neutrophil differentiation and the eosinophil-directed bias of murine bone marrow stem cells, demonstrating an unexpected subtype-specific role for H1 in granulopoiesis.

Indexed as

AnimalsBone MarrowCell DifferentiationCell LineCRISPR-Cas SystemsEosinophilsGene Expression RegulationGene Knockout TechniquesHematopoiesisHematopoietic Stem CellsHistonesHumansMiceMicroscopy, Electron, TransmissionNeutrophilsTranscription FactorsH1-1 protein, humanH1-2 protein, humanH1-3 protein, humanH1-4 protein, humanH1-5 protein, humanHistonesTranscription Factorscell differentiationdevelopmental biologyH1 linker histonehematopoiesishumanimmunologyinflammationinnate immunitylineage determinationmouseneutrophil

Identifiers

PMID32391789
PMCPMC7250579
OpenAlexW3022591129

What OpenQuestion holds

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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.