Carol Mason’s laboratory recently identified atypical refinement of neurons in the developing visual system in Fmr1 mutant mice. Here, in collaboration with Mimi Shirasu-Hiza’s laboratory, she proposes to investigate whether FMR1 in astrocytes plays a role in this phenotype and to identify the cell-type specific transcriptional changes related to this effect.

Frank McCormick will address the biochemical mechanism by which mutations in SYNGAP1 drive ASD and intellectual disability. Elucidation of the mechanism of SYNGAP1 negative regulation of RAS and its effector pathways in neurons will further our understanding of the role of this pathway in health and disease, and will shed light on potential ways in which targeted RAS pathway inhibition may be therapeutically relevant.

Sung Eun “Samuel” Kwon plans to use a recently developed optical reporter of ERK activity, combined with a neuronal activity reporter, to monitor the dynamics of ERK signaling and neuronal activity in awake-behaving SynGAP mutant mice.

While glia-neuron interactions are critical to neural functions, glial functions are molecularly ill defined in health or diseases like autism spectrum disorder (ASD). Aakanksha Singhvi aims to understand how dysregulation of KCC co-transporter functions and glial engulfment, both of which have been implicated in ASD, underlie glial control of sensory neuron shape and behavior in the model organism C. elegans.