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Related Concept Videos

Regulation of Hematopoietic Stem Cells01:01

Regulation of Hematopoietic Stem Cells

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All blood and immune cells are produced from the multipotent hematopoietic stem cells (HSCs) by the process of hematopoiesis. However, they all have a limited life span. In addition, many are depleted in immune surveillance or combatting an injury or infection. This makes blood one of the most regenerative tissues. Hematopoiesis helps replenish these blood and immune cells, restoring the body's normal functioning. However, overproduction of blood and immune cells can make them cancerous or...
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The hematopoietic stem cells or HSCs are multipotent, meaning they can differentiate and give rise to all blood and immune cells. HSCs are maintained in the quiescent stage until an external stimulus initiates their differentiation. The multipotent HSCs exist as two heterogeneous populations, long-term repopulating cells (LTRC) and short-term repopulating cells (STRC). The two HSC populations have different surface markers or receptors and are classified based on quiescence and long-term...
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Hematopoiesis

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The process of blood cell formation is called hematopoiesis. Hematopoiesis starts early during development, on the seventh day of embryogenesis. This phase of hematopoiesis is called the primitive wave, wherein the extraembryonic yolk sac allows the production of erythroid cells and endothelial cells from a common precursor called hemangioblast. The erythroid cells provide oxygen to support the growth of the rapidly dividing embryo. Hemangioblasts later develop into hematopoietic stem cells or...
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The cells of the blastocyst inner cell mass only remain pluripotent for a short time. This state of pluripotency and self-renewal can be maintained in embryonic stem (ES) cell culture by adding specific chemicals or growth factors to ensure the cells can continue dividing and later differentiate into different cell types. In some cases, the cells are grown on a feeder layer of differentiated cells, which provides the growth factors and extracellular matrix components necessary for stem cell...
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Commitment is the  process whereby stem cells:
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Notch signaling was first discovered in Drosophila melanogaster, where it is involved in cell lineage differentiation. Notch signaling regulates the maintenance and differentiation of intestinal stem cells or ISCs by controlling the expression of atonal homolog 1 or Atoh1. Atoh1 directs cells to differentiate into secretory cells.
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Related Experiment Video

Updated: Sep 8, 2025

Clonal Analysis of Embryonic Hematopoietic Stem Cell Precursors Using Single Cell Index Sorting Combined with Endothelial Cell Niche Co-culture
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CLASP2 safeguards hematopoietic stem cell properties during mouse and fish development.

Anna Klaus1, Thomas Clapes1, Laurent Yvernogeau1

  • 1Hubrecht Institute-KNAW & University Medical Center Utrecht, Uppsalalaan 8, 3584 CT Utrecht, the Netherlands.

Cell Reports
|June 15, 2022
PubMed
Summary

CLASP2 deficiency impairs hematopoietic stem cell (HSC) production and self-renewal by disrupting cell surface receptor expression. This impacts HSC stemness via altered trafficking and degradation, particularly for the c-Kit receptor.

Keywords:
CLASP2CP: Developmental biologyGolgi integrityc-Kitembryonic aortahematopoietic stem cellshemogenic endotheliumintra-aortic hematopoietic clustersmousepost-translational regulationzebrafish

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Area of Science:

  • Cell Biology
  • Developmental Biology
  • Hematopoiesis

Background:

  • Hematopoietic stem cells (HSCs) rely on cell surface receptors for self-renewal and multipotency.
  • Proper receptor expression involves complex trafficking, recycling, and degradation pathways.
  • The roles of the microtubule network and Golgi apparatus in embryonic/fetal hematopoiesis are not well understood.

Purpose of the Study:

  • To investigate the role of CLASP2, a microtubule-associated protein, in HSC development.
  • To determine the impact of CLASP2 deficiency on HSC self-renewal and stemness.
  • To elucidate the mechanisms underlying HSC dysfunction in the absence of CLASP2.

Main Methods:

  • Utilized mouse and zebrafish models to study embryonic/fetal hematopoiesis.
  • Analyzed HSC production, self-renewal, and stemness markers.
  • Investigated cell surface receptor expression, specifically c-Kit.
  • Examined cellular trafficking, lysosomal degradation, and Golgi apparatus function.

Main Results:

  • Absence of CLASP2 significantly reduced overall HSC production in both species.
  • CLASP2-deficient HSCs exhibited impaired self-renewal and loss of stemness.
  • Decreased cell surface expression of the c-Kit receptor was observed.
  • This was linked to increased lysosomal degradation and reduced plasma membrane trafficking of c-Kit.
  • Dysfunctional Golgi apparatus was identified as a potential cause in CLASP2-deficient HSCs.

Conclusions:

  • CLASP2 is crucial for maintaining HSC production, self-renewal, and stemness during development.
  • CLASP2 regulates HSC stemness through control of c-Kit receptor cell surface expression.
  • Golgi apparatus dysfunction and altered protein trafficking/degradation are key mechanisms underlying CLASP2-related HSC defects.