Fig. 6. Loss of Matr3 disrupts YY1-mediated enhancer-promoter loop formation.

a Loci characterized by enhanced YY1 occupancy exhibited increased E-E and E-P loops. Mphosph8 locus was an example of a promoter with differential YY1 binding causing EP- loop gains with neighboring MyoD, ATAC-seq peaks. Mphosph8 (highlighted by yellow line) exhibited a dual YY1-gain and Rad21-loss signature. The gene formed increased interactions (highlighted by green arcs) with Cryl1 (2), Il17d (3), Xpo4 (4), and Lats (2) (highlighted by yellow lines), which displayed MyoD and ATAC peaks at these positions. Interaction dot map further reaffirmed the positive increase in EP-loop interactions. Histograms (bottom right) indicated the interaction gain/loss scores across the whole region in the plot. b YY1-mediated EP loops changed in a H3K27ac-dependent manner in the absence of Matr3. Loop gain/loss ratios were measured. YY1 enhancers with joint H3K27Ac change (∆YY1 & ∆H3K27Ac) were more likely to demonstrate loop gains than YY1 enhancers with no H3K27Ac changes (∆YY1 & H3K27Ac). c Increased YY1 and differential H3K4me3 sites were associated with reduction of E-P loop gain. YY1-mediated EP loops changed in a H3K4me3-dependent manner in the absence of Matr3. YY1p: YY1 promoters. YY1e: YY1 enhancers. YY1 promoters with co-differential H3K4me3 (∆YY1p & ∆H3K4me3) were compared to YY1 promoters with no H3K4me3 changes (∆YY1p & H3K4me3). In (b, c) Wilcoxon’s rank-sum test (one-sided), corrected for multiple comparisons by BH method. d Sites of 4-way (ATAC-seq, Rad21, MyoD, YY1) co-differential signatures were more likely to harbor loop interaction changes. Source data are provided as a Source Data file.