Preprint (4 MB) - 
Free accessOther version: http://www.biorxiv.org/content/early/2017/12/23/236638
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Preprint
unige:101701 
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Deficient autophagy drives aging in Hydra |
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| Authors | 
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| Year | 2017 | |
| Description | 16 | |
| Abstract | Hydra exhibits a negligible senescence as its epithelial and interstitial stem cell populations continuously divide. Here we identified two H. oligactis strains that respond differently to interstitial stem cell loss. Cold-resistant (Ho_CR) animals adapt and remain healthy while coldsensitive (Ho_CS) ones die within three months, after their epithelial stem cells lose their selfrenewal potential. In Ho_CS but not in Ho_CR animals, the autophagy flux is deficient, characterized by a low induction upon starvation, proteasome inhibition or Rapamycin treatment, and a constitutively repressed Ulk activity. In the non-aging Hydra vulgaris, WIPI2 silencing suffices to induce aging. Rapamycin can delay aging by sustaining epithelial self-renewal and regeneration, although without enhancing the autophagy flux. Instead Rapamycin promotes engulfment in epithelial cells where p62/SQSTM1-positive phagocytic vacuoles accumulate. This study uncovers the importance of autophagy in the longevity of early-branched eumetazoans by maintaining stem cell renewal, and a novel anti-aging effect of Rapamycin via phagocytosis. | |
| Keywords | Hydra model system — Aging mechanisms — Regeneration — Epithelial stem cells — Autophagy — Proteostasis — Rapamycin — P62/SQSTM1 — ULK1 — WIPI2 | |
| Identifiers | DOI: 10.1101/236638 | |
| Note | supplemental file: Methods, 10 supplemental Figures, one Table and four Movies | |
| Note | Soumis dans : BioRxiv | |
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| Structures | ||
| Projects | FNS: 31003A_149630; 31003_169930 NH grant R01AG037962 | |
| Citation (ISO format) | TOMCZYK, Szymon et al. Deficient autophagy drives aging in Hydra. 2017. doi: 10.1101/236638 https://archive-ouverte.unige.ch/unige:101701 |
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