CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development
- Klaus, A., Clapes, T., Yvernogeau, L., Basu, S., Weijts, B., Maas, J., Smal, I., Galjart, N., Robin, C.
- Cell Reports 39: 110957 (Journal)
- Registered Authors
- Weijts, Bart
- 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
- Microtubule-Associated Proteins/metabolism
- Proto-Oncogene Proteins c-kit/metabolism
- Receptor Protein-Tyrosine Kinases/metabolism
- 35705037 Full text @ Cell Rep.
Klaus, A., Clapes, T., Yvernogeau, L., Basu, S., Weijts, B., Maas, J., Smal, I., Galjart, N., Robin, C. (2022) CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development. Cell Reports. 39:110957.
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
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes