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Single-cell transcriptomics identifies CD44 as a marker and regulator of endothelial to haematopoietic transition

Author

Listed:
  • Morgan Oatley

    (EMBL Rome - Epigenetics and Neurobiology Unit)

  • Özge Vargel Bölükbası

    (EMBL Rome - Epigenetics and Neurobiology Unit
    Harvard University)

  • Valentine Svensson

    (Wellcome Trust Sanger Institute
    EMBL-EBI
    California Institute of Technology)

  • Maya Shvartsman

    (EMBL Rome - Epigenetics and Neurobiology Unit)

  • Kerstin Ganter

    (EMBL Rome - Epigenetics and Neurobiology Unit)

  • Katharina Zirngibl

    (Structural and Computational Biology Unit)

  • Polina V. Pavlovich

    (EMBL Rome - Epigenetics and Neurobiology Unit
    Moscow Institute of Physics and Technology
    Max Planck Institute of Immunobiology and Epigenetics)

  • Vladislava Milchevskaya

    (Structural and Computational Biology Unit
    Institut für Medizinische Statistik und Bioinformatik)

  • Vladimira Foteva

    (EMBL Rome - Epigenetics and Neurobiology Unit)

  • Kedar N. Natarajan

    (Wellcome Trust Sanger Institute
    The University of Southern Denmark, Danish Institute for Advanced Study)

  • Bianka Baying

    (Genomics Core Facility)

  • Vladimir Benes

    (Genomics Core Facility)

  • Kiran R. Patil

    (Structural and Computational Biology Unit)

  • Sarah A. Teichmann

    (Wellcome Trust Sanger Institute)

  • Christophe Lancrin

    (EMBL Rome - Epigenetics and Neurobiology Unit)

Abstract

The endothelial to haematopoietic transition (EHT) is the process whereby haemogenic endothelium differentiates into haematopoietic stem and progenitor cells (HSPCs). The intermediary steps of this process are unclear, in particular the identity of endothelial cells that give rise to HSPCs is unknown. Using single-cell transcriptome analysis and antibody screening, we identify CD44 as a marker of EHT enabling us to isolate robustly the different stages of EHT in the aorta-gonad-mesonephros (AGM) region. This allows us to provide a detailed phenotypical and transcriptional profile of CD44-positive arterial endothelial cells from which HSPCs emerge. They are characterized with high expression of genes related to Notch signalling, TGFbeta/BMP antagonists, a downregulation of genes related to glycolysis and the TCA cycle, and a lower rate of cell cycle. Moreover, we demonstrate that by inhibiting the interaction between CD44 and its ligand hyaluronan, we can block EHT, identifying an additional regulator of HSPC development.

Suggested Citation

  • Morgan Oatley & Özge Vargel Bölükbası & Valentine Svensson & Maya Shvartsman & Kerstin Ganter & Katharina Zirngibl & Polina V. Pavlovich & Vladislava Milchevskaya & Vladimira Foteva & Kedar N. Nataraj, 2020. "Single-cell transcriptomics identifies CD44 as a marker and regulator of endothelial to haematopoietic transition," Nature Communications, Nature, vol. 11(1), pages 1-18, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-019-14171-5
    DOI: 10.1038/s41467-019-14171-5
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    Cited by:

    1. Patrick Coulombe & Grace Cole & Amanda Fentiman & Jeremy D. K. Parker & Eric Yung & Misha Bilenky & Lemlem Degefie & Patrick Lac & Maggie Y. M. Ling & Derek Tam & R. Keith Humphries & Aly Karsan, 2023. "Meis1 establishes the pre-hemogenic endothelial state prior to Runx1 expression," Nature Communications, Nature, vol. 14(1), pages 1-15, December.
    2. Brandon Hadland & Barbara Varnum-Finney & Stacey Dozono & Tessa Dignum & Cynthia Nourigat-McKay & Adam M. Heck & Takashi Ishida & Dana L. Jackson & Tomer Itkin & Jason M. Butler & Shahin Rafii & Cole , 2022. "Engineering a niche supporting hematopoietic stem cell development using integrated single-cell transcriptomics," Nature Communications, Nature, vol. 13(1), pages 1-17, December.
    3. Xia Chen & Peiliang Wang & Hui Qiu & Yonglin Zhu & Xingwu Zhang & Yaxuan Zhang & Fuyu Duan & Shuangyuan Ding & Jianying Guo & Yue Huang & Jie Na, 2022. "Integrative epigenomic and transcriptomic analysis reveals the requirement of JUNB for hematopoietic fate induction," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

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