Fig. 7: Synthetic ecteinascidins exhibit distinct patterns of chromatin binding associated with cell phenotypes.

a Left panel: Venn diagrams (n = 3) between promoters bound by Bio-lurbi and Bio-PM54 in 501mel (top) and MM029 (bottom) cells. Right panel: the two Venn diagrams were merged. b Gene tracks of Bio-lurbi, Bio-PM54, RNAPII, H3K27ac occupancy, ATAC-seq and RNA-Seq signals at CDK7 (left) or EP300 (right) loci in 501mel or MM029 cells. RNA-Seq signals show that these genes are expressed in both 501mel and MM029 melanoma cells. In blue, drug binding at promoters is highlighted. Localization of CpG islands is shown. c Left panel: Venn diagrams (n = 3) comparing genomic bindings sites uniquely bound by Bio-lurbi in either 501mel or MM029 cells with H3K27ac peaks found exclusively in either 501mel or MM029 cells. Right panel: Venn diagrams comparing genomic bindings sites uniquely bound by Bio-PM54 in either 501mel or MM029 cells with H3K27ac peaks found exclusively in either 501mel or MM029 cells. We considered different peaks as overlapping if there was at least 1 bp of overlap. d Gene tracks of Bio-lurbi, Bio-PM54, RNAPII, H3K27ac occupancy, ATAC-seq and RNA-Seq signals at the MITF locus in 501mel or MM029 cells. RNA-Seq signals show that this gene is only expressed in differentiated 501mel cells. The red square indicates the SE regulating the expression of MITF. In blue, drug binding at the promoter is highlighted. In red, drug binding at the SE is highlighted. Localization of CpG islands is shown. Note that MITF-M isoform is expressed in melanoma. e Gene tracks of Bio-lurbi, Bio-PM54, RNAPII, H3K27ac occupancy, ATAC-Seq and RNA-Seq signals at the BIRC3 locus in 501mel or MM029 cells. RNA-Seq signals show that this gene is only expressed in undifferentiated MM029 melanoma cells. In blue, drug binding at the promoter is highlighted. Localization of CpG islands is shown. f Upper panel: Venn diagrams (n = 3) comparing all genomic bindings sites commonly bound by Bio-lurbi and Bio-PM54 and bona fide super-enhancers identified in 501mel cells. Lower panel: Venn diagrams comparing all genomic bindings sites commonly bound by Bio-lurbi and Bio-PM54 and bona fide super-enhancers identified in MM029 cells.