Adhesion-mediated mechanosignaling forces mitohormesis,Cell Metabolism

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Adhesion-mediated mechanosignaling forces mitohormesis
Cell Metabolism ( IF 29.0 ) Pub Date : 2021-05-20 , DOI: 10.1016/j.cmet.2021.04.017
Kevin M Tharp ₁ , Ryo Higuchi-Sanabria ₂ , Greg A Timblin ₃ , Breanna Ford ₄ , Carlos Garzon-Coral ₅ , Catherine Schneider ₆ , Jonathon M Muncie ₁ , Connor Stashko ₁ , Joseph R Daniele ₇ , Andrew S Moore ₈ , Phillip A Frankino ₂ , Stefan Homentcovschi ₂ , Sagar S Manoli ₉ , Hao Shao ₁₀ , Alicia L Richards ₁₁ , Kuei-Ho Chen ₁₁ , Johanna Ten Hoeve ₁₂ , Gregory M Ku ₁₃ , Marc Hellerstein ₆ , Daniel K Nomura ₄ , Karou Saijo ₃ , Jason Gestwicki ₁₀ , Alexander R Dunn ₁₄ , Nevan J Krogan ₁₁ , Danielle L Swaney ₁₁ , Andrew Dillin ₂ , Valerie M Weaver ₁₅

Affiliation

Center for Bioengineering and Tissue Regeneration, Department of Surgery, University of California, San Francisco, San Francisco, CA 94143, USA.
Department of Molecular & Cellular Biology, Howard Hughes Medical Institute, University of California Berkeley, Berkeley, CA 94597, USA.
Department of Molecular and Cell Biology, University of California Berkeley, Berkeley, CA 94720, USA.
Department of Nutritional Sciences and Toxicology, University of California Berkeley, Berkeley, CA 94720, USA; Novartis, Berkeley Center for Proteomics and Chemistry Technologies and Department of Chemistry, University of California Berkeley, Berkeley, CA 94720, USA.
Chemical Engineering Department, Stanford University, Stanford, CA 94305, USA.
Novartis, Berkeley Center for Proteomics and Chemistry Technologies and Department of Chemistry, University of California Berkeley, Berkeley, CA 94720, USA.
MD Anderson Cancer Center, South Campus Research, Houston, CA 77054, USA.
Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA.
Department of Cell and Tissue Biology, University of California, San Francisco, San Francisco, CA 94143, USA.
Department of Pharmaceutical Chemistry, University of California, San Francisco, San Francisco, CA 94158, USA.
Quantitative Biosciences Institute (QBI), J. David Gladstone Institutes, Department of Cellular and Molecular Pharmacology, University of California, San Francisco, San Francisco, CA 94158, USA.
UCLA Metabolomics Center, Department of Molecular and Medical Pharmacology, University of California, Los Angeles, Los Angeles, CA 90095, USA.
Diabetes Center, Division of Endocrinology and Metabolism, Department of Medicine, UCSF, San Francisco, CA 94143, USA.
Department of Nutritional Sciences and Toxicology, University of California Berkeley, Berkeley, CA 94720, USA.
Center for Bioengineering and Tissue Regeneration, Department of Surgery, University of California, San Francisco, San Francisco, CA 94143, USA; Department of Bioengineering and Therapeutic Sciences and Department of Radiation Oncology, Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research, and The Helen Diller Family Comprehensive Cancer Center, University of California, San Francisco, San Francisco, CA 94143, USA.

Mitochondria control eukaryotic cell fate by producing the energy needed to support life and the signals required to execute programed 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 aging. However, the physical characteristics of the extracellular matrix are also altered in cancerous and aging tissues. Here, we demonstrate that cells sense the physical properties of the extracellular matrix and activate a mitochondrial stress response that adaptively tunes mitochondrial function via solute carrier family 9 member A1-dependent ion exchange and heat shock factor 1-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.

中文翻译：

粘附介导的机械信号力有丝分裂

线粒体通过产生支持生命所需的能量和执行程序性细胞死亡所需的信号来控制真核细胞的命运。已知生化环境会影响线粒体功能，并导致与癌症和衰老相关的功能失调的线粒体表型。然而，细胞外基质的物理特性也在癌变和老化组织中发生了改变。在这里，我们证明细胞感知细胞外基质的物理特性并激活线粒体应激反应，该反应通过溶质载体家族 9 成员 A1 依赖性离子交换和热休克因子 1 依赖性转录自适应地调节线粒体功能。全面的，

更新日期：2021-07-06

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