ArticleScientific reports2017
A GCSFR/CSF3R zebrafish mutant models the persistent basal neutrophil deficiency of severe congenital neutropenia.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 40 citations in OpenAlex.
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- Two axolotl-adapted cell-ablation platforms reveal macrophage-dependent processes essential for spinal-cord and skeletal regeneration.bioRxiv : the preprint server for biology · 2026Article
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- Corticosterone reprograms splenic responses to avian pathogenic Escherichia coli infection in broiler chickens.Poultry science · 2025Article
- A JAGN1-associated severe congenital neutropenia zebrafish model revealed an altered G-CSFR signaling and UPR activation.Blood advances · 2024Article
- Biallelic deleterious germlineEJHaem · 2023Article
- Zebrafish: A Relevant Genetic Model for Human Primary Immunodeficiency (PID) Disorders?International journal of molecular sciences · 2023Review
- Learning from Zebrafish Hematopoiesis.Advances in experimental medicine and biology · 2023Review
- The Early Peritoneal Cavity Immune Response toMicroorganisms · 2022Article
- Hematopoietic Cell Isolation by Antibody-Free Flow Cytometry in the Zebrafish Embryo.Methods in molecular biology (Clifton, N.J.) · 2022Article
- Leukemia-associated truncation of granulocyte colony-stimulating factor receptor impacts granulopoiesis throughout the life-course.Frontiers in immunology · 2022Article
- Vitamin D Enhances Neutrophil Generation and Function in Zebrafish (Danio rerio).Journal of innate immunity · 2022Article
- A zebrafish model for HAX1-associated congenital neutropenia.Haematologica · 2021Article
- Transcriptome Profiling of Atlantic Salmon Adherent Head Kidney Leukocytes Reveals That Macrophages Are Selectively Enriched During Culture.Frontiers in immunology · 2021Article
- Article
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- Zebrafish Granulocyte Colony-Stimulating Factor Receptor Maintains Neutrophil Number and Function throughout the Life Span.Infection and immunity · 2019Article
- Peering through zebrafish to understand inherited bone marrow failure syndromes.Haematologica · 2019Review
- Macrophages protect Talaromyces marneffei conidia from myeloperoxidase-dependent neutrophil fungicidal activity during infection establishment in vivo.PLoS pathogens · 2018Article
- Overexpression of microRNA-722 fine-tunes neutrophilic inflammation by inhibitingDisease models & mechanisms · 2017Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Granulocyte colony-stimulating factor (GCSF) and its receptor (GCSFR), also known as CSF3 and CSF3R, are required to maintain normal neutrophil numbers during basal and emergency granulopoiesis in humans, mice and zebrafish. Previous studies identified two zebrafish CSF3 ligands and a single CSF3 receptor. Transient antisense morpholino oligonucleotide knockdown of both these ligands and receptor reduces neutrophil numbers in zebrafish embryos, a technique widely used to evaluate neutrophil contributions to models of infection, inflammation and regeneration. We created an allelic series of zebrafish csf3r mutants by CRISPR/Cas9 mutagenesis targeting csf3r exon 2. Biallelic csf3r mutant embryos are viable and have normal early survival, despite a substantial reduction of their neutrophil population size, and normal macrophage abundance. Heterozygotes have a haploinsufficiency phenotype with an intermediate reduction in neutrophil numbers. csf3r mutants are viable as adults, with a 50% reduction in tissue neutrophil density and a substantial reduction in the number of myeloid cells in the kidney marrow. These csf3r mutants are a new animal model of human CSF3R-dependent congenital neutropenia. Furthermore, they will be valuable for studying the impact of neutrophil loss in the context of other zebrafish disease models by providing a genetically stable, persistent, reproducible neutrophil deficiency state throughout life.
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