<i>ser-2</i> is expressed in a subset of GABAergic motor neurons.

<p>(A) A composite DIC image with fluorescent overlay showing that the <i>Pser</i>-2::mCherry transcriptional reporter is expressed in head muscles, head neurons, and neurons in the ventral nerve cord. (B–D) Transgenic animal showing coexpression of <i>Pser-2::</i>mCherry (B) and <i>Punc-47::</i>GFP, which labels all GABAergic motor neurons (C). <i>Pser-2::</i>mCherry is strongly expressed in the GABAergic VD neurons but not the DD neurons (D). Anterior is to the left. Scale bar is 20 µm. (E) Exogenous tyramine induces immobilization though the activation of SER-2 and Gα_o signaling pathway in the GABAergic neurons. Shown is the percentage of animals that become immobilized after 10 min on 30 mM tyramine. Loss-of-function of <i>unc-25</i> (glutamic acid decarboxylase) suppresses the tyramine resistance of <i>ser-2</i> mutant animals. <i>unc-25</i> (GABA deficient) mutants and <i>unc-25; ser-2(pk1357)</i> double mutants are not resistant to the paralytic effects of exogenous tyramine. Expression of SER-2 in all GABAergic neurons (<i>Punc-47</i>::SER-2) restores sensitivity of <i>ser-2</i> mutants to exogenous tyramine. Expression of GOA-1/Gα_o or EAT-16/RGS in all GABAergic neurons (<i>Punc-47</i>::GOA-1 or <i>Punc-47</i>::EAT-16) partially restores sensitivity to exogenous tyramine in the respective <i>goa-1</i> and <i>eat-16</i> mutants. Each bar represents the mean ± SEM for at least three trials, totaling a minimum of 30 animals.