Our latest work on RAI1 was published! This project was lead by PhD student Tricia Garay, collaboration with the Sutton lab and Jones lab.
We profile bona fide transcriptional dynamics triggered by neuronal activity shifts. An integrated genomics approach including BrU-seq, combined with electrophysiology, reveals that RAI1, the Smith-Magenis syndrome protein, controls baseline synaptic strength and homeostatic synaptic upscaling by regulating the transcriptome associated with network inactivity.
Many thanks to the PRISMS Foundation for funding this study!
Read the study here: