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The Eleven‐nineteen Lysine‐rich Leukemia Gene (ELL) Couples Transcription Elongation with Epigenetic Signaling
Author(s) -
Fufa Temesgen D,
Wakano Clay,
Byun Jung S,
Haggerty Cynthia M,
ElenitobaJohnson Kojo,
Thirman Michael J,
Raffeld Mark,
Hewitt Stephen,
Gardner Kevin
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1027.2
Subject(s) - rna polymerase ii , biology , elongation factor , histone methyltransferase , epigenetics , microbiology and biotechnology , histone , histone h2a , p tefb , gene , genetics , gene expression , promoter , rna , ribosome
The human Eleven‐nineteen Lysine‐rich Leukemia gene (ELL) was first identified as a chromosomal translocation partner for the histone‐methyltransferase mixed lineage leukemia protein (MLL) and was subsequently found to be a RNA polymerase II elongation factor. Though studies in several eukaryotic models including yeast and Drosophila are beginning to shed light on ELL function, just how ELL and its oncogenic fusion with MLL influences gene regulation in mammalian systems remains to be defined. We have profiled the interaction partners of ELL in mammalian cells by sedimentation analysis, immunoprecipitation, mass spectrometry and genome location analysis. These analyses revealed that in addition to the positive transcription elongation factor b (P‐TEFb), ELL associates dynamically with various readers, writers, and erasers of the histone code. These include, the histone acetyltransferase p300, members of the histone deacetylase complex and components of the SET1 methyltransferase complex. Surprisingly, ELL undergoes a dynamic subcellular redistribution in response to mitogen stimulation, forming compartment specific complexes in the nucleus and cytosol. These findings provide new insights into the mechanisms that couple the crosstalk between transcriptional elongation and epigenetic regulation in mammalian cells. Funding: Intramural Research Program of the NCI/NIH, USA