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Alcam-a and Pdgfr-α are essential for the development of sclerotome-derived stromal cells that support hematopoiesis

Author

Listed:
  • Emi Murayama

    (Institut Pasteur, Department of Developmental & Stem Cell Biology
    INSERM
    CNRS, UMR3738)

  • Catherine Vivier

    (Institut Pasteur, Department of Developmental & Stem Cell Biology
    CNRS, UMR3738)

  • Anne Schmidt

    (Institut Pasteur, Department of Developmental & Stem Cell Biology
    CNRS, UMR3738)

  • Philippe Herbomel

    (Institut Pasteur, Department of Developmental & Stem Cell Biology
    CNRS, UMR3738)

Abstract

Mesenchymal stromal cells are essential components of hematopoietic stem and progenitor cell (HSPC) niches, regulating HSPC proliferation and fates. Their developmental origins are largely unknown. In zebrafish, we previously found that the stromal cells of the caudal hematopoietic tissue (CHT), a niche functionally homologous to the mammalian fetal liver, arise from the ventral part of caudal somites. We have now found that this ventral domain is the sclerotome, and that two markers of mammalian mesenchymal stem/stromal cells, Alcam and Pdgfr-α, are distinctively expressed there and instrumental for the emergence and migration of stromal cell progenitors, which in turn conditions the proper assembly of the vascular component of the CHT niche. Furthermore, we find that trunk somites are similarly dependent on Alcam and Pdgfr-α to produce mesenchymal cells that foster HSPC emergence from the aorta. Thus the sclerotome contributes essential stromal cells for each of the key steps of developmental hematopoiesis.

Suggested Citation

  • Emi Murayama & Catherine Vivier & Anne Schmidt & Philippe Herbomel, 2023. "Alcam-a and Pdgfr-α are essential for the development of sclerotome-derived stromal cells that support hematopoiesis," Nature Communications, Nature, vol. 14(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:14:y:2023:i:1:d:10.1038_s41467-023-36612-y
    DOI: 10.1038/s41467-023-36612-y
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    References listed on IDEAS

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