Article ID Journal Published Year Pages File Type
4321471 Neuron 2011 14 Pages PDF
Abstract

SummaryCell surface Ig superfamily proteins (IgSF) have been implicated in several aspects of neuron development and function. Here, we describe the function of a Caenorhabditis elegans IgSF protein, RIG-3. Mutants lacking RIG-3 have an exaggerated paralytic response to a cholinesterase inhibitor, aldicarb. Although RIG-3 is expressed in motor neurons, heightened drug responsiveness was caused by an aldicarb-induced increase in muscle ACR-16 acetylcholine receptor (AChR) abundance, and a corresponding potentiation of postsynaptic responses at neuromuscular junctions. Mutants lacking RIG-3 also had defects in the anteroposterior polarity of the ALM mechanosensory neurons. The effects of RIG-3 on synaptic transmission and ALM polarity were both mediated by changes in Wnt signaling, and in particular by inhibiting CAM-1, a Ror-type receptor tyrosine kinase that binds Wnt ligands. These results identify RIG-3 as a regulator of Wnt signaling, and suggest that RIG-3 has an anti-plasticity function that prevents activity-induced changes in postsynaptic receptor fields.

► Presynaptic RIG-3 inhibits activity-induced changes in postsynaptic responses ► Activity-induced delivery of ACR-16 nAChRs is enhanced in rig-3 mutants ► RIG-3 acts as an antiplasticity molecule ► RIG-3 regulates Wnt signaling

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