Gap junctions are prominent features that link immature cells in the nervous system of both invertebrates and vertebrates. The functional consequences of these interactions by gap junctions are only partly understood. We previously showed that the C. elegans AWC olfactory neurons and their surrounding neurons form a transient embryonic gap junction network composed of the innexin gap junction protein NSY-5 (Chuang et al., 2007). NSY-5 forms both functional hemichannels and intercellular gap junction channels when heterologously expressed in Xenopus oocytes, consistent with its cell-autonomous and network functions in AWC asymmetry, respectively. Communication between AWC and other cells, not just the two AWC cells,in this
nsy-5-dependent network coordinates distinct patterns of odorant receptor expression on the left and right sides of AWC neurons, leading to long-lasting changes in neuronal function. The
nsy-5 gap junctions also affect the distribution of its downstream signaling molecules including CaMKII (
unc-43) and the adaptor protein TIR-1 that have been shown to be enriched in postsynaptic regions of AWC axons (Chuang and Bargmann, 2005). In the meeting, we will present our recent results that indicate
nsy-5 gap junctions may affect subsequent chemical synapse formation and function to translate a brief embryonic communication into a permanent change. We will also report our interesting structure-function analysis of NSY-5 channels in left-right neuronal asymmetry using different
nsy-5 isoforms and the mutations identified in C. elegans
nsy-5 mutants as molecular tools. Functions of wild-type and mutant
nsy-5 isoforms are revealed by mosaic analysis and rescue ability in C. elegans, electrophysiological analysis of channel activity in Xenopus oocytes, and localization pattern of gap junction channels in cultured mammalian cells and C. elegans.