Fig. 3

Lineage-associated drug-responsive chromatin structural changes in leukaemia cells. a STED confocal microscopy analysis of the subcellular localization and co-localization of GATA1 and TET2 in OCI-M2 cells with no drug and 1 μM 5-AZA for 3 h. b STED confocal microscopy analysis of the subcellular localization and co-localization of GATA1 and TET2 in SC cells with no drug and 1 μM 5-AZA for 3 h. c Differential growth inhibition of OCI-M2 and SC leukaemia cells induced by 1 μM 5-AZA for 3 days. d A schematic illustration of the locations of the PCR primers designed in the regulatory region of SPI1/PU.1. e The PCR signals detected by 3C assays in the erythroid leukaemia cell lines, OCI-M2 and K562, and the monocytic leukaemia cell lines, SC and THP1, with no drug and 1 μM 5-AZA for 3 h. f ChIP assays with an antibody against the active form (CTD-S2P/S5P) of RNA-pol-II at the SPI1/PU.1 locus in the OCI-M2, K562, SC and THP1 cells, with no drug and 1 μM 5-AZA for 3 h. g A schematic summary of these data suggesting opposite transformations of the chromatin conformation at SPI1/PU.1 in erythroid vs. monocytic leukaemia cells in response to 5-AZA. Data are presented as the mean ± SEM of n = 3 independent samples. *P < 0.05, **P < 0.01 and ***P < 0.001 by Student’s t test