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Significance DOT1L, the only H3K79 methyltransferase in human cells, forms a complex with AF10/AF17 and ENL/AF9, is dysregulated in mixed-lineage leukemia (MLLr), and is believed to regulate transcriptional elongation without direct evidence. Here, functional genomic, proteomic, and biochemical studies aimed at an understanding of the role of DOT1L in erythroleukemic cells show no major role in elongation but, surprisingly, reveal that DOT1L evidently has a role in transcriptional initiation by recruiting initiation factor TFIID and enhancing H2B mono-ubiquitination by restricting deubiquitination by the Spt-Ada-Gcn5-acetyltransferase (SAGA) complex. The results thus implicate the DOT1L complex in transcriptional initiation and raise the intriguing possibility that MLLr leukemic fusion proteins may also promote transcriptional initiation through modified DOT1L complexes.

DOT1L complex regulates transcriptional initiation in human erythroleukemic cells