Transcriptomic analysis of cortex tissue from neuron-specific Bmal1 KO mice
The circadian clock protein Bmal1 is critical for maintain circadian transcriptional funciton and rhythms. Global deleiton of Bmal1 renders whole mice behaviorally arrhythmic. However, cell-specific deletion of Bmal1 can reveal specific transcripts regulated by Bmal1 in a cell-specific manner. Here we used a BAC-transgenic Camk2a-iCre line to delete Bmal1 in a pan-neuronal manner. This mouse has previously been shown to have widespread Bmal1 deletion in neurons and to be arrhythmic (PMID: 25525750).  We performed bulk RNAseq on cerebral cortex tissue from Camk2a-iCre+;Bmal1(fx/fx) and Cre- control littermates. Appropriate Bmal1 targets were disregulated as expetced in these mice. Pathways analysis revealed transcripts involved in Parkinson Disease and oxidative phosphorylation to be enriched. Overall design: Camk2a-iCre+;Bmal1(fx/fx) and Cre-;Bmal1(fx/fx) control mice N=3/genotype, were kept under normal 12:12 light:dark conditions until 4 months of age, then anesthetized and perfused with PBS. Cerebral cortex tissue was dissected and frozen, then later subjected to bulk RNAseq analysis. These Camk2a-iCre mice are BAG transgenic as previously described (see Izuma et al PMID: 25525750), which have pan-neuronal Bmal1 deletion and circaidan disruption.