Life-Span Extension by Axenic Dietary Restriction Is Independent of the Mitochondrial Unfolded Protein Response and Mitohormesis in Caenorhabditis elegans
| Autor: | Lea Marie Meagher, Bart P. Braeckman, Huaihan Cai, Caroline Vlaeminck, Lieselot Vandemeulebroucke, Madina Rasulova, Ineke Dhondt |
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| Rok vydání: | 2016 |
| Předmět: |
0301 basic medicine
Aging STRESS EFFICIENCY media_common.quotation_subject Longevity UPR Mitochondrion Axenic culture 03 medical and health sciences 0302 clinical medicine Life Expectancy UPRmt Mitochondrial unfolded protein response Animals Axenic Caenorhabditis elegans The Journal of Gerontology: BIOLOGICAL SCIENCES media_common Caloric Restriction Genetics Life span biology Age Factors Biology and Life Sciences Articles biology.organism_classification Phenotype Cell biology Mitochondria Oxidative Stress 030104 developmental biology C-ELEGANS Unfolded protein response Unfolded Protein Response GROWTH Geriatrics and Gerontology Reactive Oxygen Species 030217 neurology & neurosurgery |
| Zdroj: | The Journals of Gerontology Series A: Biological Sciences and Medical Sciences JOURNALS OF GERONTOLOGY SERIES A-BIOLOGICAL SCIENCES AND MEDICAL SCIENCES |
| ISSN: | 1758-535X 1079-5006 |
| Popis: | In Caenorhabditis elegans, a broad range of dietary restriction regimens extend life span to different degrees by separate or partially overlapping molecular pathways. One of these regimens, axenic dietary restriction, doubles the worm’s life span but currently, almost nothing is known about the underlying molecular mechanism. Previous studies suggest that mitochondrial stress responses such as the mitochondrial unfolded protein response (UPRmt) or mitohormesis may play a vital role in axenic dietary restriction–induced longevity. Here, we provide solid evidence that axenic dietary restriction treatment specifically induces an UPRmt response in C elegans but this induction is not required for axenic dietary restriction–mediated longevity. We also show that reactive oxygen species–mediated mitohormesis is not involved in this phenotype. Hence, changes in mitochondrial physiology and induction of a mitochondrial stress response are not necessarily causal to large increases in life span. |
| Databáze: | OpenAIRE |
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