IRK-1 Potassium Channels Mediate Peptidergic Inhibition of Caenorhabditis elegans Serotonin Neurons via a Gₒ Signaling Pathway
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Emtage-2012-IRK-1 Potassium Channels Mediate Peptidergic Inhibition of Caenorhabditis.pdf
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Author(s)
Emtage, Lesley
Aziz-Zaman, Sonya
Padovan-Merhar, Olivia
Fang-Yen, Chris
Ringstad, Niels
Horvitz, Howard Robert
Date Issued
November 2012
Journal
Journal of Neuroscience
Publisher
Society for Neuroscience
Citation
Emtage, L., S. Aziz-Zaman, O. Padovan-Merhar, H. R. Horvitz, C. Fang-Yen, and N. Ringstad. IRK-1 Potassium Channels Mediate Peptidergic Inhibition of Caenorhabditis Elegans Serotonin Neurons via a Gₒ Signaling Pathway. Journal of Neuroscience 32, no. 46 (November 14, 2012): 16285-16295.
Version
Final published version
Abstract
To identify molecular mechanisms that function in G-protein signaling, we have performed molecular genetic studies of a simple behavior of the nematode Caenorhabditis elegans, egg laying, which is driven by a pair of serotonergic neurons, the hermaphrodite-specific neurons (HSNs). The activity of the HSNs is regulated by the Gₒ-coupled receptor EGL-6, which mediates inhibition of the HSNs by neuropeptides. We report here that this inhibition requires one of three inwardly rectifying K+ channels encoded by the C. elegans genome: IRK-1. Using ChannelRhodopsin-2-mediated stimulation of HSNs, we observed roles for egl-6 and irk-1 in regulating the excitability of HSNs. Although irk-1 is required for inhibition of HSNs by EGL-6 signaling, we found that other Gₒ signaling pathways that inhibit HSNs involve irk-1 little or not at all. These findings suggest that the neuropeptide receptor EGL-6 regulates the potassium channel IRK-1 via a dedicated pool of Gₒ not involved in other Gₒ-mediated signaling. We conclude that G-protein-coupled receptors that signal through the same G-protein in the same cell might activate distinct effectors and that specific coupling of a G-protein-coupled receptor to its effectors can be determined by factors other than its associated G-proteins.
MIT Department
Massachusetts Institute of Technology. Department of Biology
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DOI of Published Version
https://doi.org/10.1523/jneurosci.2667-12.2012
