期刊
NATURE CELL BIOLOGY
卷 19, 期 6, 页码 724-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ncb3537
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资金
- National Institutes of General Medicine [R01GM112805]
- National Cancer Institute of the National Institutes of Health [P30CA086862]
- American Heart Association [AHA 16PRE26701111]
- National Institutes of Health [T32 GM067795]
- 'Fondation ARC pour la Recherche sur le Cancer' [ARC SFI20111203781]
- CNRS-AMI Mecanobio [Mecapol_2016-2017]
The response of cells to mechanical force(1-3) is a major determinant of cell behaviour and is an energetically costly event(4,5). How cells derive energy to resist mechanical force is unknown. Here, we show that application of force to E-cadherin stimulates liver kinase B1 (LKB1) to activate AMP-activated protein kinase (AMPK), a master regulator of energy homeostasis. LKB1 recruits AMPK to the E-cadherin mechanotransduction complex, thereby stimulating actomyosin contractility, glucose uptake and ATP production. The increase in ATP provides energy to reinforce the adhesion complex and actin cytoskeleton so that the cell can resist physiological forces. Together, these findings reveal a paradigm for how mechanotransduction and metabolism are linked and provide a framework for understanding how diseases involving contractile and metabolic disturbances arise.
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