Extended Data Fig. 6: CaMK2a-SUN1 FOS CUT&RUN revealed FOS binding sites across genome.
From: Bidirectional perisomatic inhibitory plasticity of a Fos neuronal network
a, Pairwise Pearson correlation between CaMK2a-SUN1 FOS CUT&RUN biological replicates for each antibody and stimulus condition. b, Histogram plotting distribution of distances between CaMK2a-SUN1 FOS CUT&RUN peaks and the nearest Refseq transcription start site (TSS). Peaks with a distance of 0 overlap the TSS. As expected42, ~90% of FOS-bound sites are distal to the TSS. c–e, Histograms plotting distributions of distances between the TSS of (c) all Refseq genes, (d) CaMK2a-Ribotag ARGs, or (e) CA1 excitatory genes downregulated with AP-1 loss (FFJ snRNA-seq), and the nearest FOS binding site. A distance of 0 indicates overlap of a FOS peak with the TSS. Notably, both CaMK2a-specific ARGs (d) and putative AP-1 targets downregulated with AP-1 loss in FFJ snRNA-seq (e) are significantly enriched for FOS-bound sites, which are significantly closer to the TSS when compared to all genes (c) (P < 2.2 × 10−16, two-sided Wilcoxon rank-sum test), providing further support that these genes are direct targets of FOS. f, Top three enriched motifs identified by MEME-ChIP from CaMK2a-SUN1 FOS CUT&RUN peaks. E-values and matching transcription factor motifs are displayed to the right of each enriched motif. FOS CUT&RUN peaks identified therefore show significant enrichment for the AP-1 motif. g–k, Tracks displaying FOS or IgG binding under 2-3 h post-vehicle or KA conditions for genomic regions surrounding the (g) Bdnf, (h) Inhba, (i) Rgs2, (j) Nptx2, or (k) Pcsk1 genes (see Fig. 4i for Scg2). y-axis shows spike-in normalized CUT&RUN coverage. Tracks are scaled to the maximum value observed for all samples for the displayed genomic locus, shown in brackets.
