Author
Listed:
- Andrea C. Carrano
(Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA)
- Zheng Liu
(Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA
The Howard Hughes Medical Institute, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
The Glenn Center for Aging Research, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)
- Andrew Dillin
(Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA
The Howard Hughes Medical Institute, The Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, California 92037, USA
The Glenn Center for Aging Research, 10010 North Torrey Pines Road, La Jolla, California 92037, USA)
- Tony Hunter
(Molecular and Cell Biology Laboratory, The Salk Institute for Biological Studies, La Jolla, California 92037, USA)
Abstract
Ubiquitination and longevity The fact that dietary restriction increases longevity in a range of different animal species suggests that there is a conserved mechanism at work. Carrano et al. now show that the E3 ubiquitin ligase WWP-1 is essential for such lifespan extension in the worm. The lifespan enhancing abilities of WWP-1 are specific to dietary restriction and require the transcription factor pha-4, and not the transcription factor daf-16 — best known for its involvement in lifespan extension via reduced insulin/IGF-1 signalling. This finding implicates the widely conserved ubiquitination pathway in the longevity response to dietary restriction.
Suggested Citation
Andrea C. Carrano & Zheng Liu & Andrew Dillin & Tony Hunter, 2009.
"A conserved ubiquitination pathway determines longevity in response to diet restriction,"
Nature, Nature, vol. 460(7253), pages 396-399, July.
Handle:
RePEc:nat:nature:v:460:y:2009:i:7253:d:10.1038_nature08130
DOI: 10.1038/nature08130
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