Our experimental approach is to use a combination of forward genetics, reverse genetics and functional genomics to identify synaptic genes, generate mutants and then assay mutant phenotypes to elucidate the function of normal synaptic gene products. Synaptic development involves specifying and constructing an intercellular communication link. The developmental program specifies synaptic partnerships and aligns the presynaptic signaling field with the postsynaptic receptor field. The mature function of the synapse is to translate electrical information into chemical information and back again. This information transfer requires mechanisms to couple an action potential to the fusion of neurotransmitter vesicles, receipt of the signal by a receptor field and downstream signaling pathways.
Synaptic plasticity is the key to nervous system adaptability, including higher cognitive functions.
An increasing interest in our laboratory is to develop Drosophila models of human neurological diseases linked to inherited synaptic dysfunction. On-going studies include a model of Fragile X Disease, the most common inherited neurological disease which results in cognitive impairment. Several lines of evidence suggest that Fragile X Disease is caused by an arrest of synaptic development due to inappropriate translational regulation. We are investigating the hypothesis that these diseases are caused by progressive loss of synaptic transmission, which is required to maintain neuronal viability. Our approach to the synapse is multi-disciplinary and requires the marriage of many traditionally distinct fields.