[
International C. elegans Meeting,
1997]
The termination of synaptic transmission is often mediated by the action of neurotransmitter transporter proteins. These transporters remove neurotransmitter from the synaptic cleft into pre-synaptic neurons and glial cells. This action is vital for the ordered functioning of the nervous system. The members of two gene families are currently thought to be responsible for this action. A third gene family is responsible for uptake of neurotransmitter into the synaptic vesicles. We are interested in members of the sodium- and chloride-dependent neurotransmitter transporter gene family. These transporters are of particular interest as they are the targets of a number of drugs, such as cocaine and Prozac, which have profound effects on the behaviour of higher mammals. We present here data we have obtained on the cloning of several neurotransmitter transporter protein genes from C. elegans. The genes are T23G5.5, a putative dopamine transporter, T13B5.1, T28F3.? and F55H12.1. All the transporter cDNA!s we have cloned are members of the gene family of sodium- and chloride-dependent neurotransmitter transporters. The members of this family all share a number of motifs; twelve putative trans-membrane domains, a large extracellular loop which contains sites for glycosylation and a conserved motif (GLGNIWRFPXXXYNGGG) between trans-membrane domains 1 and 2, thought to be important for transport function. We present the cDNA sequences of these four transporter genes and highlight the features which suggest they are members of this gene family. We also discuss the genomic structure of these genes and comment on the evolution of this gene family in C. elegans. We also present expression patterns for several of these genes and uptake studies carried out in a COS cell expression system in order to understand the roles these proteins may be playing in the nervous system of C. elegans.