Research Paper Volume 12, Issue 9 pp 8202—8220
A cellular surveillance and defense system that delays aging phenotypes in C. elegans
- 1 Center for Plant Aging Research, Institute for Basic Science, Daegu 42988, Republic of Korea
- 2 Department of New Biology, DGIST, Daegu 42988, Republic of Korea
- 3 Present address: Department of Biological Sciences, Seoul National University, Seoul 08826, Republic of Korea
Received: September 19, 2019 Accepted: February 23, 2020 Published: April 29, 2020https://doi.org/10.18632/aging.103134
How to Cite
Copyright © 2020 Hahm et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Physiological stresses, such as pathogen infection, are detected by “cellular Surveillance Activated Detoxification and Defenses” (cSADD) systems that trigger host defense responses. Aging is associated with physiological stress, including impaired mitochondrial function. Here, we investigated whether an endogenous cSADD pathway is activated during aging in C. elegans. We provide evidence that the transcription factor ZIP-2, a well-known immune response effector in C. elegans, is activated in response to age-associated mitochondrial dysfunction. ZIP-2 mitigates multiple aging phenotypes, including mitochondrial disintegration and reduced motility of the pharynx and intestine. Importantly, our data suggest that ZIP-2 is activated during aging independently of bacterial infection and of the transcription factors ATFS-1 and CEBP-2. Thus, ZIP-2 is a key component of an endogenous pathway that delays aging phenotypes in C. elegans. Our data suggest that aging coopted a compensatory strategy for regulation of aging process as a guarded process rather than a simple passive deterioration process.