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  EBF1-deficient bone marrow stroma elicits persistent changes in HSC potential

Derecka, M., Herman, J. S., Cauchy, P., Ramamoorthy, S., Lupar, E., Grün, D., et al. (2020). EBF1-deficient bone marrow stroma elicits persistent changes in HSC potential. Nature, 21, 261-273. doi:10.1038/s41590-020-0595-7.

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Dereka et al..pdf (Publisher version), 15MB
 
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 Creators:
Derecka, Marta1, Author
Herman, Josip Stefan2, Author
Cauchy, Pierre1, Author              
Ramamoorthy, Senthilkumar1, Author
Lupar, Ekaterina1, Author
Grün, Dominic2, Author              
Grosschedl, Rudolf1, Author              
Affiliations:
1Department of Cellular and Molecular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243641              
2Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243642              

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 Abstract: Crosstalk between mesenchymal stromal cells (MSCs) and hematopoietic stem cells (HSCs) is essential for hematopoietic homeostasis and lineage output. Here, we investigate how transcriptional changes in bone marrow (BM) MSCs result in long-lasting effects on HSCs. Single-cell analysis of Cxcl12-abundant reticular (CAR) cells and PDGFRα+Sca1+ (PαS) cells revealed an extensive cellular heterogeneity but uniform expression of the transcription factor gene Ebf1. Conditional deletion of Ebf1 in these MSCs altered their cellular composition, chromatin structure and gene expression profiles, including the reduced expression of adhesion-related genes. Functionally, the stromal-specific Ebf1 inactivation results in impaired adhesion of HSCs, leading to reduced quiescence and diminished myeloid output. Most notably, HSCs residing in the Ebf1-deficient niche underwent changes in their cellular composition and chromatin structure that persist in serial transplantations. Thus, genetic alterations in the BM niche lead to long-term functional changes of HSCs.

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Language(s): eng - English
 Dates: 2020-02-17
 Publication Status: Published online
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 Rev. Type: Peer
 Identifiers: DOI: 10.1038/s41590-020-0595-7
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Title: Nature
  Abbreviation : Nature
Source Genre: Journal
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Publ. Info: London : Nature Publishing Group
Pages: - Volume / Issue: 21 Sequence Number: - Start / End Page: 261 - 273 Identifier: ISSN: 0028-0836
CoNE: https://pure.mpg.de/cone/journals/resource/954925427238