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Updated: Jun 13, 2026
09:39
In Vivo Imaging of Dauer-specific Neuronal Remodeling in C. elegans
Published on: September 4, 2014
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Neuronal IL-17 controls Caenorhabditis elegans developmental diapause through CEP-1/p53.
Abhishiktha Godthi1,2, Sehee Min1,2, Srijit Das2
1Department of Cell Stress Biology, Roswell Park Comprehensive Cancer Center, Buffalo, NY 14263.
Summary
Nutrient availability, signaled by neuronal cytokine ILC-17.1, controls Caenorhabditis elegans development. This signaling suppresses CEP-1/p53 to promote growth or allows dauer arrest when absent.
Area of Science:
- Developmental Biology
- Neuroimmunology
- Metabolism
Background:
- Coordination of cell division and metabolism with nutrient availability during development is poorly understood.
- The roles of neuronal signaling in linking nutrient status to developmental fate are emerging.
Purpose of the Study:
- To investigate how nutrient availability regulates developmental transitions in Caenorhabditis elegans.
- To elucidate the molecular mechanisms linking neuronal signals, metabolism, and cell cycle control.
Main Methods:
- Utilized Caenorhabditis elegans as a model organism.
- Investigated the role of the neuronal cytokine ILC-17.1 and its downstream effector CEP-1/p53.
- Analyzed gene expression (phosphofructokinase, cytochrome C) and developmental outcomes (growth, dauer arrest).
Main Results:
- Nutrient availability, signaled by ILC-17.1, promotes glucose utilization and suppresses CEP-1/p53 activity, facilitating growth.
- Absence of ILC-17.1 activates CEP-1/p53, leading to cell-cycle inhibition and dauer larva arrest.
- Identified a novel DNA damage-independent function of CEP-1/p53 in invertebrate development.
Conclusions:
- ILC-17.1 signaling links nutrient availability and energy metabolism to cell cycle progression via CEP-1/p53.
- Revealed ancestral functions of IL-17 and p53 family proteins in development.
- Discovered a new C. elegans dauer pathway and neuroimmune mechanisms relevant to cancer research.
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