The Extended Lifespan of Caenorhabditis elegans rsks-1 Mutants Depends on the Peroxisomal Fatty Acid β-Oxidation Enzyme ACOX-1.2
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Updated: Sep 27, 2026
Dietary Supplementation of Polyunsaturated Fatty Acids in Caenorhabditis elegans
Published on: November 29, 2013
Qiu Zhao1, Rui Zhu1, Hong-Xu Guo2
1State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Key Laboratory for Southwest Microbial Diversity of the Ministry of Education, Yunnan Key Laboratory of Basic Research and Innovative Application for Green Biological Production, School of Life Science, Yunnan University, Kunming 650091, China.
Abstract:
The peroxisome has been implicated in the processes of aging and longevity regulation. Nevertheless, the mechanism by which peroxisomes regulate longevity remains far from fully elucidated. Here, we compared reactive oxygen species (ROS) levels among five long-lived Caenorhabditis elegans mutants using cross-validation with four different ROS probes and observed an increase in hydrogen peroxide (H2O2) levels in rsks-1(ok1255) mutants. Transcriptomic analysis revealed that the genes involved in peroxisomal fatty acid β-oxidation were upregulated in the rsks-1(ok1255) mutants. The imbalance of H2O2 metabolism in the rsks-1(ok1255) mutants was found to be regulated by the peroxisomal fatty acid β-oxidation enzyme ACOX-1.2. Furthermore, lifespan assays and genetic analysis of transgenic strains demonstrated that the increases in autophagy and lifespan observed in long-lived rsks-1(ok1255) mutants were suppressed by acox-1.2 RNAi. These findings uncover a previously unknown role of peroxisomal fatty acid β-oxidation in the regulation of aging and longevity.
