Diagenode

Signal-induced enhancer activation requires Ku70 to readtopoisomerase1-DNA covalent complexes.


Tan Y. et al.

Enhancer activation serves as the main mechanism regulating signal-dependent transcriptional programs, ensuring cellular plasticity, yet central questions persist regarding their mechanism of activation. Here, by successfully mapping topoisomerase I-DNA covalent complexes genome-wide, we find that most, if not all, acutely activated enhancers, including those induced by 17β-estradiol, dihydrotestosterone, tumor necrosis factor alpha and neuronal depolarization, are hotspots for topoisomerase I-DNA covalent complexes, functioning as epigenomic signatures read by the classic DNA damage sensor protein, Ku70. Ku70 in turn nucleates a heterochromatin protein 1 gamma (HP1γ)-mediator subunit Med26 complex to facilitate acute, but not chronic, transcriptional activation programs. Together, our data uncover a broad, unappreciated transcriptional code, required for most, if not all, acute signal-dependent enhancer activation events in both mitotic and postmitotic cells.

Tags
Antibody

Share this article

Published
February, 2023

Source

Products used in this publication

  • ChIP-seq Grade
    C15410337
    BRD4 Antibody
  • ChIP-seq Grade
    C15410231-100
    FOXA1 Antibody
  • Bioruptor Pico
    B01080010
    Bioruptor® Pico sonication device

Events

  • APHL 2024
    Milwaukee, Wisconsin, USA
    May 6-May 9, 2024
 See all events

News

 See all news


The European Regional Development Fund and Wallonia are investing in your future.

Extension of industrial buildings and new laboratories.


       Site map   |   Contact us   |   Conditions of sales   |   Conditions of purchase   |   Privacy policy   |   Diagenode Diagnostics