PUBLICATION
CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development
- Authors
- Klaus, A., Clapes, T., Yvernogeau, L., Basu, S., Weijts, B., Maas, J., Smal, I., Galjart, N., Robin, C.
- ID
- ZDB-PUB-220616-8
- Date
- 2022
- Source
- Cell Reports 39: 110957 (Journal)
- Registered Authors
- Weijts, Bart
- Keywords
- CLASP2, CP: Developmental biology, Golgi integrity, c-Kit, embryonic aorta, hematopoietic stem cells, hemogenic endothelium, intra-aortic hematopoietic clusters, mouse, post-translational regulation, zebrafish
- MeSH Terms
-
- Hematopoietic Stem Cells*/metabolism
- Mice
- Microtubule-Associated Proteins/metabolism
- Animals
- Zebrafish*
- PubMed
- 35705037 Full text @ Cell Rep.
Abstract
Hematopoietic stem cells (HSCs) express a large variety of cell surface receptors that are associated with acquisition of self-renewal and multipotent properties. Correct expression of these receptors depends on a delicate balance between cell surface trafficking, recycling, and degradation and is controlled by the microtubule network and Golgi apparatus, whose roles have hardly been explored during embryonic/fetal hematopoiesis. Here we show that, in the absence of CLASP2, a microtubule-associated protein, the overall production of HSCs is reduced, and the produced HSCs fail to self-renew and maintain their stemness throughout mouse and zebrafish development. This phenotype can be attributed to decreased cell surface expression of the hematopoietic receptor c-Kit, which originates from increased lysosomal degradation in combination with a reduction in trafficking to the plasma membrane. A dysfunctional Golgi apparatus in CLASP2-deficient HSCs seems to be the underlying cause of the c-Kit expression and signaling imbalance.
Genes / Markers
Figure Gallery (7 images)
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping