unc-24 mutants are forward Uncs, suggesting that
unc-24 is required for normal function of the forward movement motor circuit. Molecular cloning has shown that the UNC-24 protein is a fusion of two protein domains not previously thought to be related: an ion-channel-interacting domain found in the stomatin family of proteins, and a non-specific lipid transfer domain (Barnes et al., 1996). Using reporter constructs, we have found that
unc-24 expression occurs in a variety of cell somata in one of two modes, transiently or continuously. In the forward movement motor circuit, we could only identify very transient staining in the VBs, at the time they are making synaptic connections.
unc-24 is also expressed transiently in the
vm1 and
vm2 vulval muscles and their counterparts in the male, again during the time that these muscles become functional. Indeed, we find mutants are Egl. Transient staining is also seen in a number of other neurons. Continuous staining is seen in the Mec cells (FLPs, ALMs, AVM, PLMs, PVM, and occasionally PVDs). We find that
unc-24 mutants are Mec+ but respond abnormally to repeated light touch, and mutants are also Not. Overall, this pattern of expression suggests that
unc-24 is required to regulate synaptogenesis in some cells and synaptic function in others. We have screened 12,500 genomes for suppressors of the
unc-24 locomotory defect, and have recovered 8 recessive mutations defining 8 sun genes, which show complex interactions. Genetic analysis indicates that sun mutations are epistatic to
unc-24(0), and both sun genes and
unc-24 exhibit maternal effects. We hypothesize that UNC-24 regulates cellular excitability in a subset of neurons and muscles to alter synaptic strength during synaptogenesis in some cells or cellular responsiveness in others. We further speculate that the sun genes may define more widely expressed components regulating neuronal excitability.