Fig. 4: The chromatin occupancy of SMC1A is significantly altered in lupus inflammation.

A Volcano plot of differential genomic binding events (|log2FC| > 1, p < 0.001 generated using DESeq2) from SMC1A ChIP-sequencing analysis in SLE-like (n = 3) versus basal (n = 2) male CD14⁺ monocytes. Blue dots represent regions with reduced SMC1A binding (n = 1131) and red dots with increased SMC1A binding (n = 6839). B Stacked bar graph showing the genomic distribution of reduced (upper lane) and increased (lower lane) SMC1A binding events in SLE-like versus basal monocytes from the ChIP-seq analysis shown in (A). C Proportion of genes associated with promoter and enhancer genomic regions that demonstrate reduced (down-bound) or increased (up-bound) SMC1A binding during transition from basal to SLE-like monocytes. D Volcano plot illustrating H3K27ac signal changes (|log2FC| > 1, p < 0.001 generated using DESeq2) from ChIP-sequencing analysis in SLE-like (n = 4) versus basal (n = 3) CD14⁺ monocytes. Blue dots represent regions with reduced (n = 274), and red dots with increased (n = 502) H3K27ac signal. E Area-proportional euler diagram displaying the intersection of genes associated with differential—increased (designated with up-arrow) or reduced (designated with down-arrow)—SMC1A binding and H3K27ac signal. The majority (295 out of 440, 67%) of genes with increased H3K27ac signal showed enriched SMC1A binding. F Functional enrichment analysis (Gene Ontology terms) of genes associated with both increased SMC1A binding and increased H3K27ac signal in SLE-like compared to basal monocytes. All p-values are two-tailed.