Black widow spider venom (BWSV) is known to cause neurotransmitter release from nerve terminals due to its content of high molecular weight proteins, the latrotoxins (LTX), that are known to bind with high affinity to three neural proteins in mammals. We have established C.elegans as a model organism to study the function of the binding protein, latrophilin (a member of the class B family of G-protein coupled receptors), and its role in regulating neurotransmitter release by latrotoxins, by showing that latrophilin is required for lethality of BWSV by RNAi experiments. However, a latrophilin-knockout worm is required for determining the function of the latrophilin gene. The lat-1(ok1465) allele has a deletion of the lat-1 gene, and we know that ~97% of lat-1(ok1465) homozygous worms arrest or die before adulthood, with only 3 adult offspring per animal; moreover, there is strong interaction between the lat-1 allele and various G-protein mutants. However, it is unclear if this lethality is due to the deletion in the lat-1 gene, or to adventitious mutations introduced during the process of mutagenesis to create this allele. When transgenic worms were created with the B0457 cosmid (containing the full sequence of the lat-1 gene), they rescued the lethality of lat-1(ok1465) worms, whilst concurrent injections with the unc-54::C marker plasmid yielded six surviving adults from >80 transgenic embryos, showing that the rescue was not due to the unc-54::C. Our results show that the lat-1(ok1465) allele causes developmental lethality and also an increase in defecation cycle timing, and that the B0457 cosmid can rescue both these defects. This is strong evidence that the lat-1 gene is responsible for these defects. Current work aims to rescue the lat-1(ok1465) defects with a lat-1 cDNA construct, and to determine the role of this gene in mediating the toxicity of Black Widow Spider venom.