PUBLICATION
Csf1rb regulates definitive hematopoiesis in zebrafish
- Authors
- Dai, Y., Wu, S., Cao, C., Xue, R., Luo, X., Wen, Z., Xu, J.
- ID
- ZDB-PUB-220726-30
- Date
- 2022
- Source
- Development (Cambridge, England) 149(16): (Journal)
- Registered Authors
- Wen, Zilong, Xue, Rongtao, Xu, Jin
- Keywords
- Hematopoiesis, Hematopoietic stem and progenitor cells, Zebrafish, csf1r
- MeSH Terms
-
- Hematopoietic Stem Cells/physiology
- Zebrafish Proteins*/genetics
- Hematopoiesis/genetics
- Cell Differentiation/physiology
- Mammals
- Zebrafish*/genetics
- Animals
- PubMed
- 35876681 Full text @ Development
Citation
Dai, Y., Wu, S., Cao, C., Xue, R., Luo, X., Wen, Z., Xu, J. (2022) Csf1rb regulates definitive hematopoiesis in zebrafish. Development (Cambridge, England). 149(16).
Abstract
In vertebrates, hematopoietic stem and progenitor cells (HSPCs) are capable of self-renewal and continuously replenishing all mature blood lineages throughout life. However, the molecular signaling regulating the maintenance and expansion of HSPCs remains not fully understood. Colony-stimulating factor 1 receptor (Csf1r) is believed to be the primary regulator for myeloid lineage but not HSPC development. Here, we show a surprising role of Csf1rb, a zebrafish homolog of mammalian CSF1R, in preserving the HSPCs pool by maintaining the proliferation of HSPCs. The deficiency of csf1rb leads to a reduction in both HSPCs and their differentiated progenies, including myeloid, lymphoid, and erythroid cells at early developmental stages. Likewise, the absence of csf1rb conferred similar defects upon HSPCs and leukocytes in adulthood. Furthermore, adult hematopoietic cells from csf1rb mutants failed to repopulate immuno-deficient zebrafish. Interestingly, loss-of-function and gain-of-function assays suggested that the canonical ligands for CSF1R in zebrafish, including Csf1a, Csf1b, and Il34, were unlikely to be the ligand of Csf1rb. Thus, our data indicate a previously unappreciated role of CSF1R in maintaining HSPCs, which is independent of known ligands.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping