Rho signaling promotes cell excitability and synaptic transmission

Gα_q signaling through Trio RhoGEF and Phospholipase C effectors promotes neurotransmitter release at synapses. Whether activated Rho and Phospholipase C signaling acts through shared or independent pathways remains unclear. We use the egg-laying circuit of C. elegans, which is regulated positively by Gα_q signaling and negatively by Gα_o signaling, to determine the role of Rho GTPase in G-protein regulation of neural circuit excitability. We previously showed that Trio signals in both the presynaptic Hermaphrodite-Specific command Neurons (HSNs) and the postsynaptic egg-laying vulval muscles they innervate to promote egg laying. Here we show that its effector Rho similarly signals both pre- and post-synaptically. Expression of constitutively active Rho-1(G14V) in either the HSNs or vulval muscles increased their Ca²⁺ activity and stimulated egg laying. Conversely, reducing Rho signaling in the HSNs via expression of Rho-1(T19N) or C3 transferase expression inhibited HSN Ca²⁺ activity and egg laying. Animals lacking Rho function in HSN still had vulval muscle Ca²⁺ activity that supported contraction and egg release, although this Ca²⁺ activity lacked the enhancement associated with HSN neurotransmitter release, suggesting it was largely driven by stretch-dependent feedback. Together, these results show that Rho signals in both the HSNs and vulval muscles to promote excitability and egg laying.