A Futile Battle? Protein Quality Control and the Stress of Aging

Ryo Higuchi-Sanabria; Phillip Andrew Frankino; Joseph West Paul 3rd; Sarah Uhlein Tronnes; Andrew Dillin

doi:10.1016/j.devcel.2017.12.020

A Futile Battle? Protein Quality Control and the Stress of Aging

Dev Cell. 2018 Jan 22;44(2):139-163. doi: 10.1016/j.devcel.2017.12.020.

Authors

Ryo Higuchi-Sanabria¹, Phillip Andrew Frankino¹, Joseph West Paul 3rd¹, Sarah Uhlein Tronnes¹, Andrew Dillin²

Affiliations

¹ Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA.
² Department of Molecular and Cell Biology, Howard Hughes Medical Institute, University of California, Berkeley, Berkeley, CA 94720, USA; The Glenn Center for Aging Research, University of California, Berkeley, Berkeley, CA 94720, USA. Electronic address: dillin@berkeley.edu.

Abstract

There exists a phenomenon in aging research whereby early life stress can have positive impacts on longevity. The mechanisms underlying these observations suggest a robust, long-lasting induction of cellular defense mechanisms. These include the various unfolded protein responses of the endoplasmic reticulum (ER), cytosol, and mitochondria. Indeed, ectopic induction of these pathways, in the absence of stress, is sufficient to increase lifespan in organisms as diverse as yeast, worms, and flies. Here, we provide an overview of the protein quality control mechanisms that operate in the cytosol, mitochondria, and ER and discuss how they affect cellular health and viability during stress and aging.

Keywords: ER UPR; aging; heat-shock response; mitochondrial UPR; stress response.

Publication types

Review

MeSH terms

Aging / physiology*
Animals
Autophagy
Cytoplasm / metabolism
Endoplasmic Reticulum / metabolism
Endoplasmic Reticulum-Associated Degradation
Homeostasis
Mitochondria / metabolism
Stress, Physiological / physiology*
Unfolded Protein Response*

Abstract

Publication types

MeSH terms

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