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Doctoral thesis
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English

Hydra, a model for studying the role of injury-induced ROS signalling during regeneration and monitoring the autophagy flux in live animals

Defense date2019-06-27
Abstract

Hydra is a freshwater cnidarian polyp that regenerates any missing part after amputation. This study focuses on the potential role of injury-induced ROS signaling in triggering head regeneration. We detected immediately after mid-gastric bisection symmetrical levels of mitochondrial superoxide and asymmetrical levels of hydrogen peroxide (H2O2), higher in head-regenerating tips than in basal-regenerating ones. This asymmetry likely results from a higher superoxide dismutase (SOD) activity in head-regenerating tips while catalase is lower. Pharmacological treatments (Tiron, DPI) and transient gene silencing approaches (sod-1, catalase) indicate that signaling via mitochondrial ROS plays a role in wound healing while high levels of H2O2 are necessary for apical regeneration. Through paracrine signalling, H2O2 triggers CREB phosphorylation as well as death of interstitial cells, while H2O2 levels are amplified by apoptotic cells via a feedback loop. Thus, asymmetric ROS signaling immediately after bisection is critical to induce cell death and apical regeneration.

eng
Keywords
  • Hydra model system
  • Wound healing
  • Apical and basal regeneration
  • Epithelial layers
  • Interstitial cell lineage
  • Injury-induced ROS signals
  • ROS paracrine signaling
  • Mitochondrial superoxide
  • Hydrogen peroxide
  • ROS-induced cell death
  • Superoxide dismutase
  • Catalase
  • MitoSOX
  • Amplex-red
  • Aging
  • Biosensor
Research group
Funding
  • Autre - iGE3 PhD student salary award
  • Swiss National Science Foundation - 31003A_149630, 31003_169930
Citation (ISO format)
SUKNOVIC, Nenad Slavko. Hydra, a model for studying the role of injury-induced ROS signalling during regeneration and monitoring the autophagy flux in live animals. 2019. doi: 10.13097/archive-ouverte/unige:125593
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Creation10/19/2019 11:54:00 PM
First validation10/19/2019 11:54:00 PM
Update time03/15/2023 6:18:02 PM
Status update03/15/2023 6:18:01 PM
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