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
  • Animals
  • Hematopoiesis/genetics
  • Hematopoiesis/physiology
  • Hematopoietic Stem Cells*/metabolism
  • Mice
  • Microtubule-Associated Proteins/metabolism
  • Proto-Oncogene Proteins c-kit/metabolism
  • Receptor Protein-Tyrosine Kinases/metabolism
  • 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
Figures
Show all Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping