Transcriptomic and epigenetic characterization of PVT neurons in bipolar disorder model mouse.

We have previosuly shown that our Polg(D181A) show spontaneous depressive episodes as a result of mtDNA mutations, but we do not know the cellular mechanisms that link mtDNA mutations to behavioural changes. We hypothesized that mtDNA mutation-induced mitochondrial dysfunction in PVT causes a dysregulation of epigenetics, causing a transcriptional response which ffects neuronal function and ultimately causes the depressive phenotype. We assessed this using a combination of RNA-seq, H3K27Ac ChIP-seq, and ATAC-seq and compared our H3K27Ac results to other brain regions. Overall design: RNA-seq: 4 replicates per condition. ChIP- and ATAC seq: 2 replicates per condition.