The autophagy receptor p62/SQST-1 promotes proteostasis and longevity in C. elegans by inducing autophagy

Caroline Kumsta (), Jessica T. Chang, Reina Lee, Ee Phie Tan, Yongzhi Yang, Rute Loureiro, Elizabeth H. Choy, Shaun H. Y. Lim, Isabel Saez, Alexander Springhorn, Thorsten Hoppe, David Vilchez and Malene Hansen ()
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Caroline Kumsta: Development, Aging and Regeneration Program
Jessica T. Chang: Development, Aging and Regeneration Program
Reina Lee: Development, Aging and Regeneration Program
Ee Phie Tan: Development, Aging and Regeneration Program
Yongzhi Yang: Development, Aging and Regeneration Program
Rute Loureiro: University of Cologne
Elizabeth H. Choy: Development, Aging and Regeneration Program
Shaun H. Y. Lim: Development, Aging and Regeneration Program
Isabel Saez: University of Cologne
Alexander Springhorn: University of Cologne
Thorsten Hoppe: University of Cologne
David Vilchez: University of Cologne
Malene Hansen: Development, Aging and Regeneration Program

Nature Communications, 2019, vol. 10, issue 1, 1-12

Abstract: Abstract Autophagy can degrade cargos with the help of selective autophagy receptors such as p62/SQSTM1, which facilitates the degradation of ubiquitinated cargo. While the process of autophagy has been linked to aging, the impact of selective autophagy in lifespan regulation remains unclear. We have recently shown in Caenorhabditis elegans that transcript levels of sqst-1/p62 increase upon a hormetic heat shock, suggesting a role of SQST-1/p62 in stress response and aging. Here, we find that sqst-1/p62 is required for hormetic benefits of heat shock, including longevity, improved neuronal proteostasis, and autophagy induction. Furthermore, overexpression of SQST-1/p62 is sufficient to induce autophagy in distinct tissues, extend lifespan, and improve the fitness of mutants with defects in proteostasis in an autophagy-dependent manner. Collectively, these findings illustrate that increased expression of a selective autophagy receptor is sufficient to induce autophagy, enhance proteostasis and extend longevity, and demonstrate an important role for sqst-1/p62 in proteotoxic stress responses.

Date: 2019
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DOI: 10.1038/s41467-019-13540-4

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