This project examined the effects of the conditional knockout of the transcription factor HSF1 in striatal neurons on the proteome of synapses. HSF1 is a prolific stress-responsive transcription factor, but it has been indicated in regulating synapse stability under physiological conditions in the mammalian CNS. Here, we excised the HSF1 gee from striatal neurons and examined the effects on protein levels. We find that the loss of HSF1 specifically enhances the expression of proteins involved in synapse organization and cell-cell adhesion, while depleting mitochondrial proteins.