TY - JOUR
T1 - IRK-1 potassium channels mediate peptidergic inhibition of Caenorhabditis elegans serotonin neurons via a Go signaling pathway
AU - Emtage, Lesley
AU - Aziz-Zaman, Sonya
AU - Padovan-Merhar, Olivia
AU - Horvitz, H. Robert
AU - Fang-Yen, Christopher
AU - Ringstad, Niels
PY - 2012/11/14
Y1 - 2012/11/14
N2 - 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 hermaphroditespecific 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 inhibitHSNsinvolve 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.
AB - 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 hermaphroditespecific 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 inhibitHSNsinvolve 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.
UR - http://www.scopus.com/inward/record.url?scp=84869047681&partnerID=8YFLogxK
U2 - 10.1523/JNEUROSCI.2667-12.2012
DO - 10.1523/JNEUROSCI.2667-12.2012
M3 - Article
C2 - 23152612
AN - SCOPUS:84869047681
SN - 0270-6474
VL - 32
SP - 16285
EP - 16295
JO - Journal of Neuroscience
JF - Journal of Neuroscience
IS - 46
ER -