Fig. 7. Condensates formed by MYOCD TAD domain and FUS-IDR selectively partition the histone acetyltransferase p300, but CDT1-IDR does not.

(A) Schematic of experimental design for colocalization of p300 in MYOCD condensates. (B) Average projection of WT MYOCD or chimeric condensates in COS-7 cells with IF for endogenous p300. Scale bar, 1 μm. (C) Box plot (10 to 90%) displaying the enrichment of p300 at the center of the MYOCD condensates normalized to background intensity. P value is from one-way ANOVA with Dunnett’s multiple comparison test (P values: ns P > 0.05, ***P ≤ 0.001, ****P ≤ 0.0001). n ~ 25. (D) Schematic of Lac array cells. (E) IF for p300 (magenta) in Lac array cells expressing indicated CFP-LacI fusion. Inset is LacO locus (white shows magenta and cyan overlap). Scale bar, 5 μm. (F) IF bar chart (mean ± SD) quantifying enrichment of p300 at CFP-LacI (no fusion) or CFP-LacI with fusion (x-axis label). P values from one-way ANOVA with Dunnett’s test. (P values: ns P > 0.05, **P ≤ 0.01, ****P ≤ 0.0001). n = 22. (G) Schematic of experimental design for ChIP-seq in reprogrammed 10T1/2 cells. (H) Metagene plot of the log₂fold change compared to input control of MYOCD occupancy centered on WT MYOCD peaks compared to the empty vector control. (I) Metagene plot of the log₂fold change compared to input control of H3K27ac occupancy centered on WT MYOCD peaks compared to the empty vector control. (J) Gene tracks of MYOCD and H3K27ac ChIP-seq and RNA-seq from differentiated 10T1/2 cells expressing the indicated constructs at Actg2 locus. (K) Metagene plot of the log₂fold change compared to input control of H3K27ac occupancy centered on the TSS of genes activated by WT MYOCD.