CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development

Anna Klaus, Thomas Clapes, Laurent Yvernogeau, Sreya Basu, Bart Weijts, Joris Maas, Ihor Smal, Niels Galjart, Catherine Robin

Research output: Contribution to journal/periodicalArticleScientificpeer-review

2 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)110957
JournalCell Reports
Issue number11
Publication statusPublished - 14 Jun 2022


  • Animals
  • Hematopoiesis/genetics
  • Hematopoietic Stem Cells/metabolism
  • Mice
  • Microtubule-Associated Proteins/metabolism
  • Proto-Oncogene Proteins c-kit/metabolism
  • Receptor Protein-Tyrosine Kinases/metabolism
  • Zebrafish


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