The SKN-1/Nrf2 transcription factor can protect against oxidative stress and increase lifespan in C. elegans by distinct mechanisms
| Autor: | Alexandre Benedetto, Catherine Au, Maximillian A. Thompson, Adelaide Young, Jennifer M. A. Tullet, Emily Clark, James W. M. Green, Kathrin Schmeisser, David Gems, Ann F. Gilliat |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
0301 basic medicine
Aging media_common.quotation_subject Longevity Mutant Regulator Biology medicine.disease_cause 03 medical and health sciences Transcriptional regulation medicine Animals Caenorhabditis elegans Caenorhabditis elegans Proteins Gene Transcription factor QH581.2 media_common Short Takes Genetics fungi Gene Expression Regulation Developmental Forkhead Transcription Factors Short Take Cell Biology Metabolism Cell biology DNA-Binding Proteins Oxidative Stress 030104 developmental biology C. elegans RNA Interference transcription regulation Oxidative stress Signal Transduction Transcription Factors |
| Zdroj: | Aging Cell |
| ISSN: | 1474-9718 |
| DOI: | 10.1111/acel.12627 |
| Popis: | Summary In C. elegans, the skn‐1 gene encodes a transcription factor that resembles mammalian Nrf2 and activates a detoxification response. skn‐1 promotes resistance to oxidative stress (Oxr) and also increases lifespan, and it has been suggested that the former causes the latter, consistent with the theory that oxidative damage causes aging. Here, we report that effects of SKN‐1 on Oxr and longevity can be dissociated. We also establish that skn‐1 expression can be activated by the DAF‐16/FoxO transcription factor, another central regulator of growth, metabolism, and aging. Notably, skn‐1 is required for Oxr but not increased lifespan resulting from over‐expression of DAF‐16; concomitantly, DAF‐16 over‐expression rescues the short lifespan of skn‐1 mutants but not their hypersensitivity to oxidative stress. These results suggest that SKN‐1 promotes longevity by a mechanism other than protection against oxidative damage. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|