Live-cell p53 single-molecule binding is modulated by C-terminal acetylation and correlates with transcriptional activity

Alessia Loffreda, Emanuela Jacchetti, Sofia Antunes, Paolo Rainone, Tiziana Daniele, Tatsuya Morisaki, Marco E. Bianchi, Carlo Tacchetti () and Davide Mazza ()
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Alessia Loffreda: Centro di Imaging Sperimentale
Emanuela Jacchetti: Centro di Imaging Sperimentale
Sofia Antunes: Centro di Imaging Sperimentale
Paolo Rainone: Centro di Imaging Sperimentale
Tiziana Daniele: Centro di Imaging Sperimentale
Tatsuya Morisaki: National Cancer Institute, NIH
Marco E. Bianchi: Chromatin Dynamics Unit
Carlo Tacchetti: Centro di Imaging Sperimentale
Davide Mazza: Centro di Imaging Sperimentale

Nature Communications, 2017, vol. 8, issue 1, 1-12

Abstract: Abstract Live-cell microscopy has highlighted that transcription factors bind transiently to chromatin but it is not clear if the duration of these binding interactions can be modulated in response to an activation stimulus, and if such modulation can be controlled by post-translational modifications of the transcription factor. We address this question for the tumor suppressor p53 by combining live-cell single-molecule microscopy and single cell in situ measurements of transcription and we show that p53-binding kinetics are modulated following genotoxic stress. The modulation of p53 residence times on chromatin requires C-terminal acetylation—a classical mark for transcriptionally active p53—and correlates with the induction of transcription of target genes such as CDKN1a. We propose a model in which the modification state of the transcription factor determines the coupling between transcription factor abundance and transcriptional activity by tuning the transcription factor residence time on target sites.

Date: 2017
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DOI: 10.1038/s41467-017-00398-7

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