Academic Bibliography

 Search 200 years of publications by Ghent University researchers.
Advanced search
1 file | 4.15 MB
Add to list
  1. Search results
  2. FOXO/DAF-16 activation slows down tur...

FOXO/DAF-16 activation slows down turnover of the majority of proteins in C. elegans

Ineke Dhondt (UGent) , Vladislav A Petyuk, Huaihan Cai (UGent) , Lieselot Vandemeulebroucke, Andy Vierstraete (UGent) , Richard D Smith, Geert Depuydt (UGent) and Bart Braeckman (UGent)
(2016) CELL REPORTS. 16(11). p.3028-3040
Author
Organization
Abstract
Most aging hypotheses assume the accumulation of damage, resulting in gradual physiological decline and, ultimately, death. Avoiding protein damage accumulation by enhanced turnover should slow down the aging process and extend the lifespan. However, lowering translational efficiency extends rather than shortens the lifespan in C. elegans. We studied turnover of individual proteins in the long-lived daf-2 mutant by combining SILeNCe (stable isotope labeling by nitrogen in Caenorhabditis elegans) and mass spectrometry. Intriguingly, the majority of proteins displayed prolonged half-lives in daf-2, whereas others remained unchanged, signifying that longevity is not supported by high protein turnover. This slowdown was most prominent for translation-related and mitochondrial proteins. In contrast, the high turnover of lysosomal hydrolases and very low turnover of cytoskeletal proteins remained largely unchanged. The slowdown of protein dynamics and decreased abundance of the translational machinery may point to the importance of anabolic attenuation in lifespan extension, as suggested by the hyperfunction theory.
Keywords
LONG, SYSTEM, INHIBIT TRANSLATION, DIETARY RESTRICTION, CALORIE RESTRICTION, LONGEVITY ASSURANCE, LIFE-SPAN EXTENSION, QUANTITATIVE PROTEOMICS, OXIDATIVE STRESS, AGING CAENORHABDITIS-ELEGANS

Downloads

  • Download
    Dhondt 2016 Cell Reports v16p3028.pdf
    • full text
    • |
    • open access
    • |
    • PDF
    • |
    • 4.15 MB

Citation

Please use this url to cite or link to this publication:

MLA
Dhondt, Ineke, et al. “FOXO/DAF-16 Activation Slows down Turnover of the Majority of Proteins in C. Elegans.” CELL REPORTS, vol. 16, no. 11, 2016, pp. 3028–40, doi:10.1016/j.celrep.2016.07.088.
APA
Dhondt, I., Petyuk, V. A., Cai, H., Vandemeulebroucke, L., Vierstraete, A., Smith, R. D., … Braeckman, B. (2016). FOXO/DAF-16 activation slows down turnover of the majority of proteins in C. elegans. CELL REPORTS, 16(11), 3028–3040. https://doi.org/10.1016/j.celrep.2016.07.088
Chicago author-date
Dhondt, Ineke, Vladislav A Petyuk, Huaihan Cai, Lieselot Vandemeulebroucke, Andy Vierstraete, Richard D Smith, Geert Depuydt, and Bart Braeckman. 2016. “FOXO/DAF-16 Activation Slows down Turnover of the Majority of Proteins in C. Elegans.” CELL REPORTS 16 (11): 3028–40. https://doi.org/10.1016/j.celrep.2016.07.088.
Chicago author-date (all authors)
Dhondt, Ineke, Vladislav A Petyuk, Huaihan Cai, Lieselot Vandemeulebroucke, Andy Vierstraete, Richard D Smith, Geert Depuydt, and Bart Braeckman. 2016. “FOXO/DAF-16 Activation Slows down Turnover of the Majority of Proteins in C. Elegans.” CELL REPORTS 16 (11): 3028–3040. doi:10.1016/j.celrep.2016.07.088.
Vancouver
1.
Dhondt I, Petyuk VA, Cai H, Vandemeulebroucke L, Vierstraete A, Smith RD, et al. FOXO/DAF-16 activation slows down turnover of the majority of proteins in C. elegans. CELL REPORTS. 2016;16(11):3028–40.
IEEE
[1]
I. Dhondt et al., “FOXO/DAF-16 activation slows down turnover of the majority of proteins in C. elegans,” CELL REPORTS, vol. 16, no. 11, pp. 3028–3040, 2016.
@article{8121757,
  abstract     = {{Most aging hypotheses assume the accumulation of damage, resulting in gradual physiological decline and, ultimately, death. Avoiding protein damage accumulation by enhanced turnover should slow down the aging process and extend the lifespan. However, lowering translational efficiency extends rather than shortens the lifespan in C. elegans. We studied turnover of individual proteins in the long-lived daf-2 mutant by combining SILeNCe (stable isotope labeling by nitrogen in Caenorhabditis elegans) and mass spectrometry. Intriguingly, the majority of proteins displayed prolonged half-lives in daf-2, whereas others remained unchanged, signifying that longevity is not supported by high protein turnover. This slowdown was most prominent for translation-related and mitochondrial proteins. In contrast, the high turnover of lysosomal hydrolases and very low turnover of cytoskeletal proteins remained largely unchanged. The slowdown of protein dynamics and decreased abundance of the translational machinery may point to the importance of anabolic attenuation in lifespan extension, as suggested by the hyperfunction theory.}},
  author       = {{Dhondt, Ineke and Petyuk, Vladislav A and Cai, Huaihan and Vandemeulebroucke, Lieselot and Vierstraete, Andy and Smith, Richard D and Depuydt, Geert and Braeckman, Bart}},
  issn         = {{2211-1247}},
  journal      = {{CELL REPORTS}},
  keywords     = {{LONG,SYSTEM,INHIBIT TRANSLATION,DIETARY RESTRICTION,CALORIE RESTRICTION,LONGEVITY ASSURANCE,LIFE-SPAN EXTENSION,QUANTITATIVE PROTEOMICS,OXIDATIVE STRESS,AGING CAENORHABDITIS-ELEGANS}},
  language     = {{eng}},
  number       = {{11}},
  pages        = {{3028--3040}},
  title        = {{FOXO/DAF-16 activation slows down turnover of the majority of proteins in C. elegans}},
  url          = {{http://doi.org/10.1016/j.celrep.2016.07.088}},
  volume       = {{16}},
  year         = {{2016}},
}
Altmetric
View in Altmetric
Web of Science
Times cited: