Extended Data Fig. 9: Extended characterization of the CoREST role in chromatin accessibility.
From: Endocrine resistance and breast cancer plasticity are controlled by CoREST
a, Percentage of common and specific ATAC-seq peaks in parental and reprogrammed WT and LSD1 KO T47D. b, ATAC-seq signal in WT and LSD1-KO reprogrammed T47D (top) and cells treated with 500 nM corin for 72 h (bottom). c, Second biological replicate of SMARCC1 ChIP-seq signal in WT and LSD1 KO from analysis in Fig. 6d. d, ATAC-seq signal in reprogrammed T47D treated with 500 nM corin for 72 h at accessible sites in LSD1 KO cells that are inaccessible in WT cells. e, log2 TPM values of FOXA1 expression in WT and KO LSD1 parental and reprogrammed cells, n = 2 from biological independent experiments. Data are presented as mean values + SD, unpaired t-test, two-sided, p values (parental vs reprogrammed = 0.0008, reprogrammed WT vs KO = 0.0299). f, log2 TPM values of ESR1 in parental and reprogrammed WT and LSD1 KO T47D, n = 2 biologically independent samples Data are presented as mean values + SD, unpaired t-test, two-sided, p values (parental vs reprogrammed <0.0001, parental WT vs KO < 0.0001, reprogrammed WT vs KO = 0.0041. g, h, WB of LSD1, RCOR1, and ERα from whole cell extracts of reprogrammed WT and LSD1 KO T47D cultured for 7 days in the presence of 1 µM PRC2i EPZ6438, GSK343, and DNMTi 5-azacitidine (g) or anisomycin (h). i, Proliferation of WT and LSD1 KO reprogrammed T47D cells treated with 1 µM of tamoxifen or fulvestrant for 5 days. j, Second biological replicate of SMARCC1 ChIP-seq signal in WT and LSD1 KO from analysis in Fig. 6j. Uncropped images are available as source data.
