We are examining two social behaviors, aggression and courtship, in Drosophila to study the neural substrates of these complex behaviors as well as how organisms activate one mutually exclusive behavior over another. The Drosophila brain contains  only ~100,000 neurons providing a “simpler” brain in terms of  number and in combination with the powerful genetic toolbox  available in this organism, affords a unique opportunity to  visualize and manipulate individual neurons and distinct neural  circuits. We use genetic and immunohistochemical techniques to examine small subsets of  neurons in the adult fly brain.  To analyze whole animal behavior, we place adult  male and female flies in courtship and aggressive paradigms. 

Sex-specific Social Behavior: The daily life of an organism is  a series of decisions.  These decisions are modified through a  variety of environmental and intrinsic contexts. Our research is  directed toward understanding how neural circuits are built and  function to allow organisms to perceive the world and carry out  specific behaviors. To implement behaviors that are appropriate  for the environmental context, an organism must receive  sensory cues, assess and integrate these cues, and then execute a  behavioral program.  Aggression is an easily observable, robust  innate behavior in nearly all species including Drosophila.   Although aggression and aggressive behavioral patterns are  hardwired into the nervous system, male and females display  different aggressive patterns and aggression is also a plastic  behavior that can be modified by experience, environment, and  hormones. Currently, we are studying the octopamine (OA) neuronal  system as a key component in the male behavioral choice response.

Drosophila as a model for MeCP2 Duplication Syndrome: A second project in the lab is addressing fundamental mechanisms of MeCP2 function in microcircuit function and regulation of MeCP2 expression in glial cells. Methyl-CpG-binding protein 2 (MeCP2) is one of the most dosage-sensitive genes involved in neuronal functional integrity. Altered levels of MeCP2 either through loss-of-function mutations (Rett Syndrome (RTT)) or increased protein levels due to gene duplication (MeCP2 Duplication Snydrome), result in dramatic phenotypes including mental retardation, motor dysfunction, features of autism, stereotyped hand movements, and sleep disturbances, and are known collectively as MeCP2 spectrum disorders (MSD). Using Drosophila as a model organism, we are elucidating the cell-type specific effects of MeCP2 function on microcircuits controlling sleep behavior, utilizing high-resolution 3D imaging to examine microcircuit synaptic connections, and undertaking genomic approaches to identify gene products which down-regulate astrocytic MeCP2 expression. Understanding how mutations in MeCP2 or altered MeCP2 protein levels affects neuron, microcircuits, and target gene expression will provide insight into a large group of MeCP2-associated disorders.