AF4 uses the SL1 components of RNAP1 machinery to initiate MLL fusion- and AEP-dependent transcription

Hiroshi Okuda, Akinori Kanai, Shinji Ito, Hirotaka Matsui and Akihiko Yokoyama ()
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Hiroshi Okuda: Laboratory for Malignancy Control Research, Kyoto University Graduate School of Medicine
Akinori Kanai: Research Institute for Radiation Biology and Medicine, Hiroshima University
Shinji Ito: Medical Research Support Center, Kyoto University Graduate School of Medicine
Hirotaka Matsui: Research Institute for Radiation Biology and Medicine, Hiroshima University
Akihiko Yokoyama: Laboratory for Malignancy Control Research, Kyoto University Graduate School of Medicine

Nature Communications, 2015, vol. 6, issue 1, 1-12

Abstract: Abstract Gene rearrangements generate MLL fusion genes, which can lead to aggressive leukemia. In most cases, MLL fuses with a gene encoding a component of the AEP (AF4 family/ENL family/P-TEFb) coactivator complex. MLL–AEP fusion proteins constitutively activate their target genes to immortalize haematopoietic progenitors. Here we show that AEP and MLL–AEP fusion proteins activate transcription through selectivity factor 1 (SL1), a core component of the pre-initiation complex (PIC) of RNA polymerase I (RNAP1). The pSER domain of AF4 family proteins associates with SL1 on chromatin and loads TATA-binding protein (TBP) onto the promoter to initiate RNA polymerase II (RNAP2)-dependent transcription. These results reveal a previously unknown transcription initiation mechanism involving AEP and a role for SL1 as a TBP-loading factor in RNAP2-dependent gene activation.

Date: 2015
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DOI: 10.1038/ncomms9869

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