Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1
| Autor: | Petra Hoffmann, Matthias Edinger, Andreas Schmidt, Magda Babina, Sandra Schmidhofer, Gernot Längst, Andreas Fuchs, Michael Rehli, Johanna Raithel, Rudolf Schill, Claudia Gebhard, Dagmar Glatz, Rainer Spang, Margit Nützel, Anna Ratermann, Christian Schmidl, Karina Mendes, Julia Minderjahn, Axel Imhof |
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| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Cell type Science Protein domain genetic processes Gene regulatory network 610 Medizin General Physics and Astronomy RNA-Seq Chromatin remodelling Biology General Biochemistry Genetics and Molecular Biology Article 03 medical and health sciences 0302 clinical medicine Redistribution (chemistry) lcsh:Science Transcription factor ddc:610 Multidisciplinary General Chemistry humanities Chromatin Cell biology Gene regulation Nucleosomes 030104 developmental biology Haematopoiesis lcsh:Q Reprogramming Transcription 030217 neurology & neurosurgery |
| Zdroj: | Nature Communications, Vol 11, Iss 1, Pp 1-16 (2020) Nature Communications |
| ISSN: | 2041-1723 |
| DOI: | 10.1038/s41467-019-13960-2 |
| Popis: | 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. PU.1 is a master TF of hematopoietic lineage differentiation. Here the authors analyse properties of PU.1 DNA-binding in vitro and genome-wide in vivo across different cell types with native or ectopic PU.1 expression, and uncover the mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1. |
| Databáze: | OpenAIRE |
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