RT Journal Article
SR Electronic
T1 Adhesion-mediated mechanosignaling forces mitohormesis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 2020.03.06.979583
DO 10.1101/2020.03.06.979583
A1 Kevin M. Tharp
A1 Ryo Higuchi-Sanabria
A1 Greg A. Timblin
A1 Breanna Ford
A1 Carlos Garzon-Coral
A1 Catherine Schneider
A1 Jonathon M. Muncie
A1 Connor Stashko
A1 Joseph R. Daniele
A1 Andrew S. Moore
A1 Phillip A. Frankino
A1 Sagar S. Manoli
A1 Hao Shao
A1 Alicia L. Richards
A1 Kuei-Ho Chen
A1 Gregory M. Ku
A1 Marc Hellerstein
A1 Daniel K. Nomura
A1 Karou Saijo
A1 Jason Gestwicki
A1 Alexander R. Dunn
A1 Nevan J. Krogan
A1 Danielle L. Swaney
A1 Andrew Dillin
A1 Valerie M. Weaver
YR 2020
UL http://biorxiv.org/content/early/2020/10/25/2020.03.06.979583.abstract
AB Mitochondria control eukaryotic cell fate by producing the energy needed to support life and the signals required to execute programmed cell death. The biochemical milieu is known to affect mitochondrial function and contribute to the dysfunctional mitochondrial phenotypes implicated in cancer and the morbidities of ageing. However, the physical characteristics of the extracellular matrix are also altered in cancer and in aging tissues. We demonstrate that cells sense the physical properties of the extracellular matrix and activate a mitochondrial stress response that adaptively tunes mitochondrial function via SLC9A1-dependent ion exchange and HSF1-dependent transcription. Overall, our data indicate that adhesion-mediated mechanosignaling may play an unappreciated role in the altered mitochondrial functions observed in aging and cancer.Competing Interest StatementThe authors have declared no competing interest.