造血干細胞對高能和氧化壓力非常敏感，對它們的靜止與增殖之間的平衡進行調控是響應代謝壓力,、同時保持其長期再生能力所需要的。三項新的研究表明,，腫瘤抑制因子和代謝傳感器Lkb1在維持造血細胞的能量平衡中起關鍵作用,。Lkb1被發(fā)現是細胞周期調控及能量平衡所必需的，造血干細胞對Lkb1的依賴性要強于對任何其他造血細胞的依賴性,。（生物谷Bioon.com）
生物谷推薦原文出處：
Nature doi:10.1038/nature09571
Lkb1 regulates cell cycle and energy metabolism in haematopoietic stem cells
Daisuke Nakada1,2, Thomas L. Saunders2,3 & Sean J. Morrison1,2
1.Howard Hughes Medical Institute, Life Sciences Institute, Center for Stem Cell Biology, University of Michigan, Ann Arbor, Michigan 48109-2216, USA
2.Department of Internal Medicine, University of Michigan, Ann Arbor, Michigan 48109-2216, USA
3.Transgenic Animal Model Core, University of Michigan, Ann Arbor, Michigan 48109-2216, USA
Top of pageAbstractLittle is known about metabolic regulation in stem cells and how this modulates tissue regeneration or tumour suppression. We studied the Lkb1 tumour suppressor and its substrate AMP-activated protein kinase (AMPK), kinases that coordinate metabolism with cell growth. Deletion of the Lkb1 (also called Stk11) gene in mice caused increased haematopoietic stem cell (HSC) division, rapid HSC depletion and pancytopenia. HSCs depended more acutely on Lkb1 for cell-cycle regulation and survival than many other haematopoietic cells. HSC depletion did not depend on mTOR activation or oxidative stress. Lkb1-deficient HSCs, but not myeloid progenitors, had reduced mitochondrial membrane potential and ATP levels. HSCs deficient for two catalytic α-subunits of AMPK (AMPK-deficient HSCs) showed similar changes in mitochondrial function but remained able to reconstitute irradiated mice. Lkb1-deficient HSCs, but not AMPK-deficient HSCs, exhibited defects in centrosomes and mitotic spindles in culture, and became aneuploid. Lkb1 is therefore required for HSC maintenance through AMPK-dependent and AMPK-independent mechanisms, revealing differences in metabolic and cell-cycle regulation between HSCs and some other haematopoietic progenitors.
