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PAK2 links cell survival to mechanotransduction and metabolism
Journal article   Open access   Peer reviewed

PAK2 links cell survival to mechanotransduction and metabolism

Hannah K. Campbell, Alicia M. Salvi, Timothy O'Brien, Richard Superfine and Kris A. DeMali
The Journal of cell biology, Vol.218(6), pp.1958-1971
06/01/2019
DOI: 10.1083/jcb.201807152
PMCID: PMC6548143
PMID: 30940647
url
https://doi.org/10.1083/jcb.201807152View
Published (Version of record) Open Access

Abstract

Too little or too much force can trigger cell death, yet factors that ensure the survival of cells remain largely unknown. Here, we demonstrate that E-cadherin responds to force by recruiting and activating p21-activated protein kinase 2 (PAK2) to allow cells to stiffen, metabolize, and survive. Interestingly, PAK2 activation and its control of the apoptotic response are specific for the amplitude of force applied. Specifically, under low amplitudes of physiological force, PAK2 is protected from proteolysis, thereby ensuring cell survival. In contrast, under higher amplitudes of physiological force, PAK2 is left unprotected and stimulates apoptosis, an effect that is prevented by cleavage-resistant forms of the protein. Finally, we demonstrate that PAK2 protection is conferred by direct binding of AMPK. Thus, PAK2 mediates the survival of cells under force. These findings reveal an unexpected paradigm for how mechanotransduction, metabolism, and cell survival are linked.
Cell Biology Life Sciences & Biomedicine Science & Technology

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