ArticleExperimental hematology2016
Spliceosomal component Sf3b1 is essential for hematopoietic differentiation in zebrafish.
Article in Experimental hematology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Prpf4 sequentially regulates the expansion and maturation of erythrocyte through distinct mechanisms.Cell death discovery · 2025Article
- SMC2 and Condensin II Subunits Are Essential for the Development of Hematopoietic Stem and Progenitor Cells in Zebrafish.Journal of cellular physiology · 2025Article
- SF3B1K700E mutation in human embryonic stem cells causes aberrant expression of immune-related genes.PloS one · 2025Article
- The splicing factor Prpf31 is required for hematopoietic stem and progenitor cell expansion during zebrafish embryogenesis.The Journal of biological chemistry · 2024Article
- Splicing factor deficits render hematopoietic stem and progenitor cells sensitive to STAT3 inhibition.Cell reports · 2022Article
- Cytogenetic and Genetic Abnormalities with Diagnostic Value in Myelodysplastic Syndromes (MDS): Focus on the Pre-Messenger RNA Splicing Process.Diagnostics (Basel, Switzerland) · 2022Review
- Ddx41 inhibition of DNA damage signaling permits erythroid progenitor expansion in zebrafish.Haematologica · 2022Article
- Two oppositely-charged sf3b1 mutations cause defective development, impaired immune response, and aberrant selection of intronic branch sites in Drosophila.PLoS genetics · 2021Article
- A splicing factor switch controls hematopoietic lineage specification of pluripotent stem cells.EMBO reports · 2021Article
- Spliceosomopathies: Diseases and mechanisms.Developmental dynamics : an official publication of the American Association of Anatomists · 2020Review
- Modeling hematopoietic disorders in zebrafish.Disease models & mechanisms · 2019Review
- The splicing factor Sf3b1 regulates erythroid maturation and proliferation via TGFβ signaling in zebrafish.Blood advances · 2019Article
- RES complex is associated with intron definition and required for zebrafish early embryogenesis.PLoS genetics · 2018Article
- Spliceosomal components protect embryonic neurons from R-loop-mediated DNA damage and apoptosis.Disease models & mechanisms · 2018Article
- Modeling Myeloid Malignancies Using Zebrafish.Frontiers in oncology · 2017Review
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
SF3B1 (Splicing factor 3b, subunit 1) is one of the most commonly mutated factors in myelodysplastic syndrome (MDS). Although the genetic correlation between SF3B1 mutations and MDS etiology are quite strong, no in vivo model currently exists to explore how SF3B1 loss alters blood cell development. Using zebrafish mutants, we show here that proper function of Sf3b1 is required for all hematopoietic lineages. As in MDS patients, zebrafish sf3b1 mutants develop a macrocytic-anemia-like phenotype due to a block in maturation at a late progenitor stage. The mutant embryos also develop neutropenia, because their primitive myeloid cells fail to mature and turn on differentiation markers such as l-plastin and myeloperoxidase. In contrast, production of definitive hematopoietic stem and progenitor cells (HSPCs) from hemogenic endothelial cells within the dorsal aorta is greatly diminished, whereas arterial endothelial cells are correctly fated. Notch signaling, imperative for the endothelial-to-hematopoietic transition, is also normal, indicating that HSPC induction is blocked in sf3b1 mutants downstream or independent of Notch signaling. The data demonstrate that Sf3b1 function is necessary during key differentiation fate decisions in multiple blood cell types. Zebrafish sf3b1 mutants offer a novel animal model with which to explore the role of splicing in hematopoietic development and provide an excellent in vivo system with which to delve into the question of why and how Sf3b1 dysfunction is detrimental to hematopoietic differentiation, which could improve MDS diagnosis and treatment.
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