Acoustic communication and social behavior of Drosophila melanogaster

Drosophila melanogaster offers an arsenal of molecular genetic tools to identify the functions of individual genes and proteins, their interaction partners within cellular/molecular pathways and their impact on physiology and behavioral performance. Making use of this large variety of genetic methods to manipulate the formation and function of its nervous system, studies on Drosophila have increased our knowledge about nervous development, plasticity including learning and memory formation and the control of sexually dimorphic complex interactive behaviours like courtship and aggression.

Human neuro-developmental disorders such as autism spectrum disorders, schizophrenia, attention deficit hyperactivity disorders and Tourette syndrome are believed to result from interplay of multiple genetic risk factors with environmental stimuli. In many cases defects in synaptogenesis, synaptic maintenance and plasticity account for phenotypes that include deficits in social behavior, communication and cognitive functions. Drosophila’s behaviour, including its well-decribed social behavior, is increasingly used to study mechanisms underlying heritable human neuro-developmental disorders, pinpointing the contribution of genetic risk factors for these conditions. As one example, we expose neuroligin 2-deficient Drosophila to behavioural tests addressing their social interactions, space-dispersal, and behavioural switching and analysed their acoustic communication patterns.



Neuroligins are a family of phylogenetically conserved postsynaptic adhesion molecules whose intracellular domains bind to synaptic scaffolding proteins while extracellular domains assemble with presynaptic Neurexins. Mutations in neuroligin genes have been identified as risk factors for the development of autism spectrum disorders (ASDs). We show that deletion of the dnl2 gene, coding for one of four Neuroligin isoforms, alters acoustic communication signals, affects the transition between different behaviours and impairs social interactions in Drosophila melanogaster. dnl2-deficient flies maintain larger distances to conspecifics and males perform less female-directed courtship and male-directed aggressive behaviours while the patterns of these behaviours and general locomotor activity resembled those of wild type controls. Since olfactory, visual and auditory perception were not altered in dnl2-deficient mutants, reduced social interactions seem to result from altered excitability in central nervous neuropils that initiate social behaviours. Our results demonstrate that neuroligins are phylogenetically conserved not only regarding their structure and direct function at the synapse but also with respect to their fine-tuning of synaptic function in brain circuits that regulate social behaviours which seems to date back to common ancestors of humans and flies.