Article abstract
Nature Neuroscience 11, 1168 - 1176 (2008)
Published online: 21 September 2008 | doi:10.1038/nn.2186
FMRFamide neuropeptides and acetylcholine synergistically inhibit egg-laying by C. elegans
Niels Ringstad1 & H Robert Horvitz1
Abstract
Egg-laying behavior of the Caenorhabditis elegans hermaphrodite is regulated by G protein signaling pathways. Here we show that the egg laying–defective mutant egl-6(n592) carries an activating mutation in a G protein–coupled receptor that inhibits C. elegans egg-laying motor neurons in a Go-dependent manner. Ligands for EGL-6 are Phe-Met-Arg-Phe-NH2 (FMRFamide)-related peptides encoded by the genes flp-10 and flp-17. flp-10 is expressed in both neurons and non-neuronal cells. The major source of flp-17 peptides is a pair of presumptive sensory neurons, the BAG neurons. Genetic analysis of the egl-6 pathway revealed that the EGL-6 neuropeptide signaling pathway functions redundantly with acetylcholine to inhibit egg-laying. The retention of embryos in the uterus of the C. elegans hermaphrodite is therefore under the control of a presumptive sensory system and is inhibited by the convergence of signals from neuropeptides and the small-molecule neurotransmitter acetylcholine.
- Howard Hughes Medical Institute, McGovern Institute for Brain Research, Department of Biology, 68-425, Massachusetts Institute of Technology, 77 Massachusetts Avenue, Cambridge, Massachusetts 02139, USA.
Correspondence to: H Robert Horvitz1 e-mail: horvitz@mit.edu
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