TY - JOUR
T1 - Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1
AU - Minderjahn, Julia
AU - Schmidt, Andreas
AU - Fuchs, Andreas
AU - Schill, Rudolf
AU - Raithel, Johanna
AU - Babina, Magda
AU - Schmidl, Christian
AU - Gebhard, Claudia
AU - Schmidhofer, Sandra
AU - Mendes, Karina
AU - Ratermann, Anna
AU - Glatz, Dagmar
AU - Nützel, Margit
AU - Edinger, Matthias
AU - Hoffman, Petra
AU - Spang, Rainer
AU - Längst, Gernot
AU - Imhof, Axel
AU - Rehli, Michael
N1 - Funding Information:
We thank Rüdiger Eder and Jaqueline Dirmeier for their support in FACS analyses, Simone Thomas for sharing methods, Sven Heinz for sharing methods and commenting on the manuscript, and Christopher Benner for comments on the manuscript. This study was funded by grants of the DFG to M.R. (RE 1310/17) and G.L. (LA 1331/17). ChIP-and RNA-sequencing were conducted at the biomedical sequencing facility (BSF) of the CeMM (Vienna; Austria), at the KFB (Kompetenzzentrum Fluoreszente Bioanalytik; Regensburg; Germany) and the NGS Core of the Regensburg Center for Interventional Immunology (RCI, University Regensburg and University Medical Center Regensburg, Germany).
Publisher Copyright:
© 2020, The Author(s).
PY - 2020/12/1
Y1 - 2020/12/1
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=85078143548&partnerID=8YFLogxK
U2 - 10.1038/s41467-019-13960-2
DO - 10.1038/s41467-019-13960-2
M3 - Article
C2 - 31964861
AN - SCOPUS:85078143548
SN - 2041-1723
VL - 11
JO - Nature Communications
JF - Nature Communications
IS - 1
M1 - 402
ER -