Abstract

The Drosophila neuromuscular junction (NMJ) is a glutamatergic synapse that is structurally and functionally similar to mammalian glutamatergic synapses. These synapses can, as a result in changes in activity, alter the strength of their connections via processes that require chromatin remodeling and changes in gene expression. The chromodomain helicase binding domain (CHD) protein Kismet (Kis) is expressed in both the presynaptic motor neuron nuclei and postsynaptic muscle nuclei of the Drosophila NMJ. Here we show that Kis is involved in the localization and clustering of glutamate receptors in postsynaptic muscle cells, in the proper morphology of presynaptic motor neurons, in larval motor behavior, and in synaptic transmission. Our data suggests that Kis is part of the machinery that modulates the development and function of this synapse. Kis is the homolog to human CHD7, which is mutated in CHARGE syndrome. Thus, our data may suggest novel avenues of investigation for synaptic defects associated with CHARGE syndrome.%%%%Ph.D., Biological Sciences – Drexel University, 2014

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