Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1

Julia Minderjahn, Andreas Schmidt, Andreas Fuchs, Rudolf Schill, Johanna Raithel, Magda Babina, Christian Schmidl, Claudia Gebhard, Sandra Schmidhofer, Karina Mendes, Anna Ratermann, Dagmar Glatz, Margit Nützel, Matthias Edinger, Petra Hoffmann, Rainer Spang, Gernot Längst, Axel Imhof and Michael Rehli ()
Additional contact information
Julia Minderjahn: University Hospital Regensburg
Andreas Schmidt: Ludwig-Maximilians-Universität München
Andreas Fuchs: University of Regensburg
Rudolf Schill: University of Regensburg
Johanna Raithel: University Hospital Regensburg
Magda Babina: Charité Universitätsmedizin Berlin
Christian Schmidl: University Regensburg and University Medical Center Regensburg
Claudia Gebhard: University Hospital Regensburg
Sandra Schmidhofer: University Hospital Regensburg
Karina Mendes: University Hospital Regensburg
Anna Ratermann: University Hospital Regensburg
Dagmar Glatz: University Hospital Regensburg
Margit Nützel: University Hospital Regensburg
Matthias Edinger: University Hospital Regensburg
Petra Hoffmann: University Hospital Regensburg
Rainer Spang: University of Regensburg
Gernot Längst: University of Regensburg
Axel Imhof: Ludwig-Maximilians-Universität München
Michael Rehli: University Hospital Regensburg

Nature Communications, 2020, vol. 11, issue 1, 1-16

Abstract: Abstract Establishing gene regulatory networks during differentiation or reprogramming requires master or pioneer transcription factors (TFs) such as PU.1, a prototype master TF of hematopoietic lineage differentiation. To systematically determine molecular features that control its activity, here we analyze DNA-binding in vitro and genome-wide in vivo across different cell types with native or ectopic PU.1 expression. Although PU.1, in contrast to classical pioneer factors, is unable to access nucleosomal target sites in vitro, ectopic induction of PU.1 leads to the extensive remodeling of chromatin and redistribution of partner TFs. De novo chromatin access, stable binding, and redistribution of partner TFs both require PU.1’s N-terminal acidic activation domain and its ability to recruit SWI/SNF remodeling complexes, suggesting that the latter may collect and distribute co-associated TFs in conjunction with the non-classical pioneer TF PU.1.

Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-019-13960-2

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DOI: 10.1038/s41467-019-13960-2

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