한빛사논문
Ukjin Choi 1,2,5, Mingxi Hu 2,5, Qixin Zhang 3 & Derek Sieburth 2,4,*
1DSR graduate program, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
2Zilkha Neurogenetic Institute, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
3MPHY program, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
4Department of Physiology and Neuroscience, Keck School of Medicine, University of Southern California, Los Angeles, CA 90033, USA.
5These authors contributed equally: Ukjin Choi, Mingxi Hu.
*Corresponding author: correspondence to Derek Sieburth
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.
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