The pharynx, is divided into three functional compartments: the corpus, the isthmus, and the terminal bulb (TB). In C. elegans the corpus and the TB are connected via gap junctions, resulting in synchronous contractions of these compartments. Feeding behavior is regulated by 20 pharyngeal neurons. In different nematode species, different subsets of synapses function to regulate feeding behavior. In C. elegans, M4 innervates the isthmus and the TB and is necessary for proper isthmus function, but has no detectable TB function. In P. redivivus the TB is capable of pumping independently of the corpus. This behavior is not present in C. elegans and it requires the motor neuron M4. So we propose that different subsets of M4 synapses are acting to regulate feeding behavior in C. elegans and P. redivivus. Our analysis of
slo-1 mutants in C. elegans suggests that differential activity of M4TB synapses between the two species is due to differences in synaptic strength. SLO-1 is a Ca-activated K channel.
slo-1 mutants have novel M4 dependent EPSPs on EPGs (electrical recordings of the corpus and TB).
slo-1 mutants have increased TB pumping in an
eat-5 background (loss of
eat-5 isolates the TB electrically by inactivating gap junctions between the corpus and TB), and M4 and M5 are the only known neurons to innervate the TB.
slo-1 has been shown to increase synaptic transmission at body wall NMJs (Wang et. al. 2000). We interpret our results as activation of the normally silent M4TB synapses in
slo-1 mutants. Thus, simply by increasing synaptic transmission, C. elegans M4TB synapses can be made functionally similar to proposed homologous synapses in P. redivivus. This raises the possibility that
slo-1 may be important in the functional evolution of M4TB synapses. In addition to activating the M4TB synapse,
slo-1 has another interesting phenotype.
eat-5 mutants grow slowly on DA837 (hard to eat E. coli).
slo-1 suppresses the growth rate defect of
eat-5 on DA837, likely due to increased TB pumping. To find other genes that may activate the M4TB synapse we screened for
eat-5 suppressors and identified
unc-2 and
unc-36. UNC-2 and UNC-36 are Ca channel subunits, suggesting a role for voltage-gated Ca channels in the silencing of the M4TB synapse. Since SLO-1 is a Ca-activated K channel, we believe that UNC-2 and UNC-36 may be acting upstream of SLO-1. This result is surprising since mutations in these genes would be expected to decrease synaptic transmission. We hypothesize that other Ca channels are important for synaptic transmission at the M4TB synapse.