Signal-induced enhancer activation requires Ku70 to read topoisomerase1–DNA covalent complexes

Author:

Tan YuliangORCID,Yao LuORCID,Gamliel Amir,Nair Sreejith J.,Taylor Havilah,Ohgi Kenny,Aggarwal Aneel K.ORCID,Rosenfeld Michael G.ORCID

Abstract

AbstractEnhancer 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.

Publisher

Springer Science and Business Media LLC

Subject

Molecular Biology,Structural Biology

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