Extended Data Fig. 5: Loss of RBMX and RBMXL1 results in a dysregulated chromatin state in leukemia cells.
a, Immunoblot analysis of RBMX/L1, MYC, and HOXA9 in RBMX/L1 depleted MOLM13 cells. The experiment was performed 3 times with similar results. b, Heatmap of the top 1,000 peaks from ATAC-sequencing from control and RBMX/L1-knockdown MOLM13 cells. n = 3 independent experiments. c, Scatterplot showing accessibility changes at pericentric and telomeric heterochromatin upon RBMX/L1-knockdown. n = 3 independent experiments. d, Location of increased accessible and decreased accessible ATAC-sequencing peaks in RBMX/L1-knockdown MOLM13 cells. e, Location of increased accessible and decreased accessible ATAC-sequencing pericentric and telomeric heterochromatin peaks in RBMX/L1-knockdown MOLM13 cells. f, Gene expression heatmap of the top 99 upregulated and downregulated genes from RNA-sequencing analysis of MOLM13 cells upon RBMX/L1 knockdown. n = 4 independent experiments. g, Tables showing alternative splicing events and genes MOLM13 cells upon RBMX/L1 depletion. n = 4 independent experiments. h, mRNA expression of the 11 genes from the overlap in Fig. 7a. n = 4 independent experiments; data as mean ± s.e.m, two-tailed Student’s t test. i, qRT-PCR of recovered RNA in RNA-IP at 11 candidate target genes shown in Fig. 7a. n = 4 independent experiments; data as mean ± s.e.m, two-tailed Student’s t test. j, Overall survival analysis of AML patients with low versus high expression of RBMX/L1 direct regulated pathway including 8 down-regulated targets validated by PAR-CLIP, RNA-IP and RNA-sequencing (CBX5, CBS, DACH1, SEPT11, UNG, XBP1, PABPC4, and SLC38A1). Data from TCGA database.
