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 Hoffman; Rainer Spang; Gernot Längst; Axel Imhof; Michael Rehli

doi:10.1038/s41467-019-13960-2

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 Hoffman, Rainer Spang, Gernot Längst, Axel Imhof, Michael Rehli^*

^*Autor correspondente para este trabalho

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78 Citações (Scopus)

Resumo

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.

Idioma original	English
Número do artigo	402
Revista	Nature Communications
Volume	11
Número de emissão	1
DOIs	https://doi.org/10.1038/s41467-019-13960-2
Estado da publicação	Publicado - 1 dez. 2020
Publicado externamente	Sim

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1 Errata

Author Correction: Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1 (Nature Communications, (2020), 11, 1, (402), 10.1038/s41467-019-13960-2)
Minderjahn, J., Schmidt, A., Fuchs, A., Schill, R., Raithel, J., Babina, M., Schmidl, C., Gebhard, C., Schmidhofer, S., Mendes, K., Ratermann, A., Glatz, D., Nützel, M., Edinger, M., Hoffmann, P., Spang, R., Längst, G., Imhof, A. & Rehli, M., 1 dez. 2020, Em: Nature Communications. 11, 1, 1139.
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Minderjahn, J., Schmidt, A., Fuchs, A., Schill, R., Raithel, J., Babina, M., Schmidl, C., Gebhard, C., Schmidhofer, S., Mendes, K., Ratermann, A., Glatz, D., Nützel, M., Edinger, M., Hoffman, P., Spang, R., Längst, G., Imhof, A., & Rehli, M. (2020). Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1. Nature Communications, 11(1), Artigo 402. https://doi.org/10.1038/s41467-019-13960-2

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title = "Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1",

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{\textquoteright}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.",

author = "Julia Minderjahn and Andreas Schmidt and Andreas Fuchs and Rudolf Schill and Johanna Raithel and Magda Babina and Christian Schmidl and Claudia Gebhard and Sandra Schmidhofer and Karina Mendes and Anna Ratermann and Dagmar Glatz and Margit N{\"u}tzel and Matthias Edinger and Petra Hoffman and Rainer Spang and Gernot L{\"a}ngst and Axel Imhof and Michael Rehli",

note = "Funding Information: We thank R{\"u}diger 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: {\textcopyright} 2020, The Author(s).",

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Minderjahn, J, Schmidt, A, Fuchs, A, Schill, R, Raithel, J, Babina, M, Schmidl, C, Gebhard, C, Schmidhofer, S, Mendes, K, Ratermann, A, Glatz, D, Nützel, M, Edinger, M, Hoffman, P, Spang, R, Längst, G, Imhof, A & Rehli, M 2020, 'Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1', Nature Communications, vol. 11, n.º 1, 402. https://doi.org/10.1038/s41467-019-13960-2

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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.

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AN - SCOPUS:85078143548

SN - 2041-1723

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JO - Nature Communications

JF - Nature Communications

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ER -

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

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Author Correction: Mechanisms governing the pioneering and redistribution capabilities of the non-classical pioneer PU.1 (Nature Communications, (2020), 11, 1, (402), 10.1038/s41467-019-13960-2)

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