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Related Experiment Video

Updated: Jun 11, 2026

Defining Hsp33's Redox-regulated Chaperone Activity and Mapping Conformational Changes on Hsp33 Using Hydrogen-deuterium Exchange Mass Spectrometry

Defining Hsp33's Redox-regulated Chaperone Activity and Mapping Conformational Changes on Hsp33 Using Hydrogen-deuterium Exchange Mass Spectrometry

Published on: June 7, 2018

Redox regulation, gene expression and longevity.

Yoko Honda¹, Masashi Tanaka, Shuji Honda

¹Department of Genomics for Longevity and Health, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan. yhonda@center.tmig.or.jp

Geriatrics & Gerontology International

|July 2, 2010

Summary

Genetic mutations in Caenorhabditis elegans can extend lifespan. Manganese superoxide dismutase (MnSOD) genes fine-tune longevity regulation, acting as redox-signaling modulators rather than antioxidants.

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Lipid Supplementation for Longevity and Gene Transcriptional Analysis in Caenorhabditis elegans

Lipid Supplementation for Longevity and Gene Transcriptional Analysis in Caenorhabditis elegans

Published on: December 9, 2022

Area of Science:

Aging research
Genetics
Molecular biology

Background:

Lifespan extension is achievable through genetic and environmental factors.
The insulin/IGF-I signaling pathway, particularly the daf-2 gene mutation, significantly extends lifespan in C. elegans.
The transcription factor DAF-16 regulates downstream targets, but their precise role in longevity is unclear.

Purpose of the Study:

To investigate the role of Manganese Superoxide Dismutase (MnSOD) isoforms (sod-2 and sod-3) in regulating lifespan and oxidative stress response in C. elegans.
To determine if oxidative stress is a limiting factor in the extended lifespan of daf-2 mutants.
To elucidate the function of MnSOD as potential targets of DAF-16 in aging.

Main Methods:

Utilized C. elegans models with double deletions in sod-2 and sod-3 genes within a daf-2 mutant background.
Assessed lifespan and oxidative stress sensitivity in genetically modified worms.
Analyzed the impact of sod-3 gene deletion on the lifespan of daf-2 mutants.

Main Results:

Double deletion of sod-2 and sod-3 genes caused oxidative-stress sensitivity but did not shorten the lifespan of daf-2 mutants.
Deletion of the sod-3 gene alone further extended the lifespan of daf-2 mutants.
These findings suggest oxidative stress is not the sole determinant of longevity in this model.

Conclusions:

MnSOD systems in C. elegans modulate insulin/IGF-I signaling-mediated longevity.
MnSOD isoforms function as physiological-redox-signaling modulators, not primarily as antioxidants, in the context of aging.
The study refines the understanding of molecular mechanisms underlying lifespan extension.