Figure 6
Figure 6. DOT1L directly regulates expression of Hoxa and Meis1 genes in MLL-AF9–transformed cells. (A) RT-qPCR analysis shows up-regulation of Hoxa cluster and their cofactors Meis1 and Pbx3, normalized to Gapdh, in MLL-AF9–transformed cells, which become down-regulated on DOT1L deletion. (B) RT-qPCR analysis shows down-regulation of myeloid differentiation markers, normalized to Gapdh, in MLL-AF9–transformed cells, which become up-regulated on DOT1L deletion. (C) ChIP analysis demonstrates that H3K79me2/3 is specifically enriched at Hoxa loci in MLL-AF9–transformed cells compared with control HPCs. IgG was used for control ChIP and amplicon positions are indicated (TSS indicates transcription start site). (D) ChIP analysis demonstrates that H3K79me2/3 is enriched in the Meis1 gene in MLL-AF9 LCs compared with that in the control HPCs. IgG was used for control ChIP and amplicon positions are indicated (TSS indicates transcription start site).

DOT1L directly regulates expression of Hoxa and Meis1 genes in MLL-AF9–transformed cells. (A) RT-qPCR analysis shows up-regulation of Hoxa cluster and their cofactors Meis1 and Pbx3, normalized to Gapdh, in MLL-AF9–transformed cells, which become down-regulated on DOT1L deletion. (B) RT-qPCR analysis shows down-regulation of myeloid differentiation markers, normalized to Gapdh, in MLL-AF9–transformed cells, which become up-regulated on DOT1L deletion. (C) ChIP analysis demonstrates that H3K79me2/3 is specifically enriched at Hoxa loci in MLL-AF9–transformed cells compared with control HPCs. IgG was used for control ChIP and amplicon positions are indicated (TSS indicates transcription start site). (D) ChIP analysis demonstrates that H3K79me2/3 is enriched in the Meis1 gene in MLL-AF9 LCs compared with that in the control HPCs. IgG was used for control ChIP and amplicon positions are indicated (TSS indicates transcription start site).

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