GSE97980
Impaired locomotor behavior of C. elegans neuroligin mutants is dependent of the catechol-O-methyltransferase COMT-4
Neuroligins are neuronal membrane adhesion molecules that have been involved in neuro-psychiatric and neuro-developmental disorders. They interact with neurexins and other specific proteins in the synaptic cleft. The nlg-1 gene of Caenorhabditis elegans encodes NLG-1, an ortholog of human neuroligins. NLG-1 is involved in dopaminergic and serotoninergic signaling that controls the locomotory rate of the nematode. When well fed animals are transferred to a plate with food (bacterial lawn) they reduce the locomotory rate. This behavior, which depends on dopamine, is known as basal slowing response (BSR). Alternatively, food deprived animals when moved to a plate with a bacterial lawn, further decrease their locomotory rate. This behavior, known as enhanced slowing response (ESR) is serotonin dependent. C. elegans nlg-1- deficient mutants are impaired in BSR, ESR and other locomotory behaviors such as gentle touch response. Here we report that nlg-1 mutants upregulate the expression of comt-4 which encodes an enzyme that presumably has catechol-O-methyltransferase activity involved in dopamine degradation. Our study also shows that comt-4(RNAi) in nlg-1-deficient mutants recovers wild type phenotypes of BSR, ESR and gentle touch responses. Based on these results we propose a model for the neuroligin function in modulating the dopamine-dependent locomotory behavior in the nematode. Overall design: Examination of differentially expressed RNAs between Caenorhabditis elegans N2 wild type strain and the nrx-1 (tm1961), nlg-1 (ok259)  and nrx-1; nlg-1 (tm1961; ok259) double mutants.