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. Author manuscript; available in PMC: 2023 May 7.
Published in final edited form as: Nat Struct Mol Biol. 2022 Nov 7;29(11):1122–1135. doi: 10.1038/s41594-022-00856-x

Extended Data Fig. 9. Extended characterization of the CoREST role in chromatin accessibility.

Extended Data Fig. 9

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 500nM corin for 72h (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 500nM corin for 72h 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 1µM PRC2i EPZ6438, GSK343, and DNMTi 5-azacitidine (g) or anisomycin (h). i, Proliferation of WT and LSD1 KO reprogrammed T47D cells treated with 1µM 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.