Electrostatic repulsion causes anticooperative DNA binding between tumor suppressor ETS transcription factors and JUN-FOS at composite DNA sites.
作者： Bethany J. Madison , Kathleen A. Clark , Niraja Bhachech , Peter C. Hollenhorst , Barbara J. Graves
关键词:
摘要: Many different transcription factors (TFs) regulate gene expression in a combinatorial fashion, often by binding close proximity to each other on composite cis-regulatory DNA elements. Here, we investigated how ETS TFs bind with the AP1 JUN–FOS at DNA-binding sites. ability correlated phenotype of proteins prostate cancer. We found that oncogenic ETS-related (ERG) and variant (ETV) 1/4/5 subfamilies co-occupy ETS–AP1 sites vitro, whereas robustly inhibited tumor suppressors homologous factor (EHF) SAM pointed domain–containing TF (SPDEF). EHF bound tighter affinity than ERG absence JUN–FOS, possibly enabling compete for Genome-wide mapping EHF- ERG-binding epithelial cells revealed is preferentially excluded from closely spaced sequences. Structural modeling mutational analyses indicated adjacent positively charged surfaces use electrostatic repulsion disfavor simultaneous binding. Conservation positive residues interface identified E74-like 1 (ELF1) as an additional exhibiting anticooperative ELF1 frequently down-regulated In summary, divergent features their enable distinct events sites, which may drive specific targeting facilitate transcriptional programs.
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