Our research follows the central hypothesis that de novo protein synthesis in neurons is a fundamental requirement for learning, and dysregulation of this process is a core contributor to autism and intellectual disability (ASD/ID). Our research questions are being investigated in multiple neural circuits using biochemical, electrophysiological and systems-level approaches.
Current projects include:
Determining the mechanisms that control local protein synthesis downstream of NMDA receptors
Tracking activity dependent changes in mRNA translation using cell type-specific Translating Ribosome Affinity Purification (TRAP) and RNA-seq
Investigating the role of protein turnover in synaptic plasticity and function
We are studying these basic biological questions using animal models of Fragile X Syndrome, SYNGAP1 Happloinsufficency, Tuberous Sclerosis, and other neurodevelopmental disorders. It is our belief that identifying the mechanisms that go awry in these models will simultaneously address fundamental questions of synaptic function, and provide a better understanding of autism and ID.