Genetic interaction of and in regulation of glutamatergic synaptogenesis.

Synaptic development and functionality have been considered as fundamental mechanisms underlying a range of neuropsychiatric disorders, including schizophrenia. Emerging evidence from biological and clinical studies implicates mutations in the gene in the pathogenesis of schizophrenia. In this study, genetic interactions among a select set of risk factor genes are examined using the unique model system: neuromuscular junctions (NMJs) in . We found that , the homolog of the human , which encodes the NLGN1 protein, genetically interacts with in synaptic development. We show that overexpression in the heterozygous background causes synaptic alterations at the NMJs that are distinct from those in the wild-type background. Loss of enhanced the overexpression phenotype in synaptic formation, strongly suppressing the formation of synaptic boutons. These results thus suggest an intriguing converging mechanism regulated by and in the developing glutamatergic synapses.