The Lkb1 metabolic sensor maintains haematopoietic stem cell survival View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2010-12

AUTHORS

Sushma Gurumurthy, Stephanie Z. Xie, Brinda Alagesan, Judith Kim, Rushdia Z. Yusuf, Borja Saez, Alexandros Tzatsos, Fatih Ozsolak, Patrice Milos, Francesco Ferrari, Peter J. Park, Orian S. Shirihai, David T. Scadden, Nabeel Bardeesy

ABSTRACT

Haematopoietic stem cells (HSCs) can convert between growth states that have marked differences in bioenergetic needs. Although often quiescent in adults, these cells become proliferative upon physiological demand. Balancing HSC energetics in response to nutrient availability and growth state is poorly understood, yet essential for the dynamism of the haematopoietic system. Here we show that the Lkb1 tumour suppressor is critical for the maintenance of energy homeostasis in haematopoietic cells. Lkb1 inactivation in adult mice causes loss of HSC quiescence followed by rapid depletion of all haematopoietic subpopulations. Lkb1-deficient bone marrow cells exhibit mitochondrial defects, alterations in lipid and nucleotide metabolism, and depletion of cellular ATP. The haematopoietic effects are largely independent of Lkb1 regulation of AMP-activated protein kinase (AMPK) and mammalian target of rapamycin (mTOR) signalling. Instead, these data define a central role for Lkb1 in restricting HSC entry into cell cycle and in broadly maintaining energy homeostasis in haematopoietic cells through a novel metabolic checkpoint. More... »

PAGES

659

References to SciGraph publications

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nature09572

DOI

http://dx.doi.org/10.1038/nature09572

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1049865214

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21124451


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