Autism Spectrum Disorder (ASD) is, at once, one of the most common developmental disorders in the world and one of the most debilitating, however, its exact causes remain poorly understood. A preliminary genetic screen has identified the gene CaMKI as a molecular candidate involved in ASD. We hypothesize that mutations in CaMKI would lead to ASD-phenotypes such as sociability deficits and aberrant synaptic refinement. Using Drosophila as a model organism, we genetically ablated CaMKI and used a social assay to measure any resulting social impairment in adult flies, a hallmark of ASD in humans. Additionally, the role of CaMKI in synaptic refinement was tested at the larval neuromuscular junction (NMJ) as well as in the central nervous system. Furthermore, we live-imaged CaMKI-null embryos expressing the genetically encoded calcium indicator GCAMP to examine the activity pattern of the nociceptive class-IV (C4da) sensory cells. Our results suggest that this activity pattern is necessary for the proper development of neuronal networks, so any irregularities provide direct evidence of impeded maturation via synaptic refinement. This study explores the relationship between CaMKI and ASD which casts light on any connection between the disorder and developmental synaptic refinement, as a whole.
This work was funded, in part, through an Undergraduate Research Award from the UMBC Division of Undergraduate Academic Affairs.