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*

*Corresponding author for this work

Research output: Contribution to journalArticleAcademicpeer-review

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.

Original languageEnglish
Article number110957
JournalCell Reports
Volume39
Issue number11
DOIs
Publication statusPublished - 14 Jun 2022

Bibliographical note

Publisher Copyright: © 2022 The Author(s)

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