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2016
- doi: 10.1038/ncomms13125
- issn: 2041-1723
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info:eu-repo/semantics/altIdentifier/doi/10.1038/ncomms13125
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info:eu-repo/semantics/altIdentifier/pmid/27731316
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info:eu-repo/semantics/altIdentifier/eissn/2041-1723
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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_9CF125118D0C3
info:eu-repo/semantics/openAccess , CC BY 4.0 , https://creativecommons.org/licenses/by/4.0/
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Progenitor cells Mother cells Colony-forming units (Cells) Primary metabolism Anabolism Metabolism, Primary Catabolism Marrow Medulla ossium Glucolysis Cultural sociology Culture--Social aspects Sociology of cultureCiter ce document
N. Vannini et al., « Specification of haematopoietic stem cell fate via modulation of mitochondrial activity. », Serveur académique Lausannois, ID : 10.1038/ncomms13125
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Haematopoietic stem cells (HSCs) differ from their committed progeny by relying primarily on anaerobic glycolysis rather than mitochondrial oxidative phosphorylation for energy production. However, whether this change in the metabolic program is the cause or the consequence of the unique function of HSCs remains unknown. Here we show that enforced modulation of energy metabolism impacts HSC self-renewal. Lowering the mitochondrial activity of HSCs by chemically uncoupling the electron transport chain drives self-renewal under culture conditions that normally induce rapid differentiation. We demonstrate that this metabolic specification of HSC fate occurs through the reversible decrease of mitochondrial mass by autophagy. Our data thus reveal a causal relationship between mitochondrial metabolism and fate choice of HSCs and also provide a valuable tool to expand HSCs outside of their native bone marrow niches.
