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Updated: Jul 14, 2026
Dissecting and Recording from The C. Elegans Neuromuscular Junction
Published on: February 25, 2009
The head mesodermal cell couples FMRFamide neuropeptide signaling with rhythmic muscle contraction in C. elegans
Ukjin Choi1,2, Mingxi Hu2, Qixin Zhang3
1DSR graduate program, Keck School of Medicine, University of Southern California, Los Angeles, CA, 90033, USA.
Abstract:
FMRFamides are evolutionarily conserved neuropeptides that play critical roles in behavior, energy balance, and reproduction. Here, we show that FMRFamide signaling from the nervous system is critical for the rhythmic activation of a single cell of previously unknown function, the head mesodermal cell (hmc) in C. elegans. Behavioral, calcium imaging, and genetic studies reveal that release of the FLP-22 neuropeptide from the AVL neuron in response to pacemaker signaling activates hmc every 50 s through an frpr-17 G protein-coupled receptor (GPCR) and a protein kinase A signaling cascade in hmc. hmc activation results in muscle contraction through coupling by gap junctions composed of UNC-9/Innexin. hmc activation is inhibited by the neuronal release of a second FMRFamide-like neuropeptide, FLP-9, which functions through its GPCR, frpr-21, in hmc. This study reveals a function for two opposing FMRFamide signaling pathways in controlling the rhythmic activation of a target cell through volume transmission.
Insights
FMRFamide neuropeptides control a C. elegans cell
Area of Science:
- Neuroscience
- Cell Biology
- Developmental Biology
Background:
- FMRFamides are conserved neuropeptides regulating behavior, energy, and reproduction.
- Their role in precise cellular activation is not fully understood.
Purpose of the Study:
- To investigate the function of FMRFamide signaling in controlling rhythmic cellular activation in C. elegans.
- To identify the specific neuropeptides, receptors, and downstream pathways involved.
Main Methods:
- Behavioral analysis
- Calcium imaging
- Genetic studies in C. elegans
- Investigated neuropeptide signaling pathways
Main Results:
- Identified FLP-22 neuropeptide release activating the head mesodermal cell (hmc) via the frpr-17 GPCR and protein kinase A.
- Demonstrated hmc activation triggers muscle contraction via UNC-9/Innexin gap junctions.
- Showed FLP-9 neuropeptide inhibits hmc activation through the frpr-21 GPCR.
Conclusions:
- Two opposing FMRFamide signaling pathways regulate rhythmic hmc activation.
- This reveals a novel mechanism of cellular control through volume transmission.
