Fig. 1: Heroin exposure increases chromatin accessibility of neuronal promoters. | Nature Communications

Fig. 1: Heroin exposure increases chromatin accessibility of neuronal promoters.

From: Chromatin accessibility mapping of the striatum identifies tyrosine kinase FYN as a therapeutic target for heroin use disorder

Fig. 1

a Schematic of the experimental design. Putamen and nucleus accumbens tissue (blue shades) was collected from post-mortem brains of human heroin users and controls. ATAC-seq was performed in FANS-sorted neuronal and non-neuronal (predominantly glial) cell populations (n = 10/group). Neuronal cells (blue tracks) showed accessible regions at the CAMK2A gene but not at glial marker OLIG2. Conversely, the OLIG2 locus but not the CAMK2A locus was accessible in non-neuronal cells (green tracks). b Neuronal ATAC peaks from heroin users were specifically enriched in CpG islands, promoters and 5′UTRs, whereas centromeres, introns, gaps, and intergenic areas were depleted across all groups (Fisher’s exact test, Benjamini–Hochberg correction). c Heat map showing the most enriched regulatory elements from ENCODE in neurons and non-neuronal cells from heroin users and control subjects. Neuronal ATAC peaks from heroin users were enriched for enhancer regions marked by H3K4me1 and EZH2 binding sites. Acb nucleus accumbens, Put putamen, Cd nucleus caudatus, utr untranslated region, ncRNA non-coding RNA.

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