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Scientific article
Open access
English

Autophagy in Hydra: a response to starvation and stress in early animal evolution

Published inBiochimica et biophysica acta, vol. 1793, no. 9, p. 1432-1443
Publication date2009
Abstract

The Hydra polyp provides a powerful model system to investigate the regulation of cell survival and cell death in homeostasis and regeneration as Hydra survive weeks without feeding and regenerates any missing part after bisection. Induction of autophagy during starvation is the main surviving strategy in Hydra as autophagic vacuoles form in most myoepithelial cells after several days. When the autophagic process is inhibited, animal survival is actually rapidly jeopardized. An appropriate regulation of autophagy is also essential during regeneration as Hydra RNAi knocked-down for the serine protease inhibitor Kazal-type (SPINK) gene Kazal1, exhibit a massive autophagy after amputation that rapidly compromises cell and animal survival. This excessive autophagy phenotype actually mimics that observed in the mammalian pancreas when SPINK genes are mutated, highlighting the paradigmatic value of the Hydra model system for deciphering pathological processes. Interestingly autophagy during starvation predominantly affects ectodermal epithelial cells and lead to cell survival whereas Kazal1(RNAi)-induced autophagy is restricted to endodermal digestive cells that rapidly undergo cell death. This indicates that distinct regulations that remain to be identified, are at work in these two contexts. Cnidarian express orthologs for most components of the autophagy and TOR pathways suggesting evolutionarily-conserved roles during starvation.

Keywords
  • Animals
  • Autophagy
  • Biological Evolution
  • Cell Survival
  • Hydra/cytology/genetics/physiology
  • Signal Transduction
  • Stress, Physiological
Research group
Funding
  • Swiss National Science Foundation - 3100A0-116784
Citation (ISO format)
CHERA, Simona et al. Autophagy in Hydra: a response to starvation and stress in early animal evolution. In: Biochimica et biophysica acta, 2009, vol. 1793, n° 9, p. 1432–1443. doi: 10.1016/j.bbamcr.2009.03.010
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Article (Published version)
accessLevelPublic
Identifiers
ISSN of the journal0006-3002
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