C/EBPα Activates Pre-existing and De Novo Macrophage Enhancers during Induced Pre-B Cell Transdifferentiation and Myelopoiesis
Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation,...
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| Published in: | Stem cell reports Vol. 5; no. 2; pp. 232 - 247 |
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| Main Authors: | , , , , , , , , , , , , |
| Format: | Journal Article |
| Language: | English |
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Elsevier Inc
11.08.2015
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| ISSN: | 2213-6711, 2213-6711 |
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| Abstract | Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation, C/EBPα binds to two types of myeloid enhancers in B cells: pre-existing enhancers that are bound by PU.1, providing a platform for incoming C/EBPα; and de novo enhancers that are targeted by C/EBPα, acting as a pioneer factor for subsequent binding by PU.1. The order of factor binding dictates the upregulation kinetics of nearby genes. Pre-existing enhancers are broadly active throughout the hematopoietic lineage tree, including B cells. In contrast, de novo enhancers are silent in most cell types except in myeloid cells where they become activated by C/EBP factors. Our data suggest that C/EBPα recapitulates physiological developmental processes by short-circuiting two macrophage enhancer pathways in pre-B cells.
[Display omitted]
•C/EBPα activates two classes of prospective myeloid enhancers in B cells•Pre-existing enhancers are bound by PU.1 and become hyper-activated by C/EBPα•C/EBPα acts as a pioneer factor with delayed kinetics on de novo enhancers•The two types of enhancers direct myeloid cell fate in B cells and hematopoiesis
In this study, Graf and colleagues show that, during B-cell-to-macrophage transdifferentiation, C/EBPα activates two types of myeloid enhancers in B cells. The two enhancer types are differentially activated, dictating gene expression levels of macrophage genes during the conversion of B cells into macrophages and normal hematopoiesis. |
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| AbstractList | Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation, C/EBPα binds to two types of myeloid enhancers in B cells: pre-existing enhancers that are bound by PU.1, providing a platform for incoming C/EBPα; and de novo enhancers that are targeted by C/EBPα, acting as a pioneer factor for subsequent binding by PU.1. The order of factor binding dictates the upregulation kinetics of nearby genes. Pre-existing enhancers are broadly active throughout the hematopoietic lineage tree, including B cells. In contrast, de novo enhancers are silent in most cell types except in myeloid cells where they become activated by C/EBP factors. Our data suggest that C/EBPα recapitulates physiological developmental processes by short-circuiting two macrophage enhancer pathways in pre-B cells.
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C/EBPα activates two classes of prospective myeloid enhancers in B cells
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Pre-existing enhancers are bound by PU.1 and become hyper-activated by C/EBPα
•
C/EBPα acts as a pioneer factor with delayed kinetics on de novo enhancers
•
The two types of enhancers direct myeloid cell fate in B cells and hematopoiesis
In this study, Graf and colleagues show that, during B-cell-to-macrophage transdifferentiation, C/EBPα activates two types of myeloid enhancers in B cells. The two enhancer types are differentially activated, dictating gene expression levels of macrophage genes during the conversion of B cells into macrophages and normal hematopoiesis. Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation, C/EBPα binds to two types of myeloid enhancers in B cells: pre-existing enhancers that are bound by PU.1, providing a platform for incoming C/EBPα; and de novo enhancers that are targeted by C/EBPα, acting as a pioneer factor for subsequent binding by PU.1. The order of factor binding dictates the upregulation kinetics of nearby genes. Pre-existing enhancers are broadly active throughout the hematopoietic lineage tree, including B cells. In contrast, de novo enhancers are silent in most cell types except in myeloid cells where they become activated by C/EBP factors. Our data suggest that C/EBPα recapitulates physiological developmental processes by short-circuiting two macrophage enhancer pathways in pre-B cells.Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation, C/EBPα binds to two types of myeloid enhancers in B cells: pre-existing enhancers that are bound by PU.1, providing a platform for incoming C/EBPα; and de novo enhancers that are targeted by C/EBPα, acting as a pioneer factor for subsequent binding by PU.1. The order of factor binding dictates the upregulation kinetics of nearby genes. Pre-existing enhancers are broadly active throughout the hematopoietic lineage tree, including B cells. In contrast, de novo enhancers are silent in most cell types except in myeloid cells where they become activated by C/EBP factors. Our data suggest that C/EBPα recapitulates physiological developmental processes by short-circuiting two macrophage enhancer pathways in pre-B cells. Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation, C/EBPα binds to two types of myeloid enhancers in B cells: pre-existing enhancers that are bound by PU.1, providing a platform for incoming C/EBPα; and de novo enhancers that are targeted by C/EBPα, acting as a pioneer factor for subsequent binding by PU.1. The order of factor binding dictates the upregulation kinetics of nearby genes. Pre-existing enhancers are broadly active throughout the hematopoietic lineage tree, including B cells. In contrast, de novo enhancers are silent in most cell types except in myeloid cells where they become activated by C/EBP factors. Our data suggest that C/EBPα recapitulates physiological developmental processes by short-circuiting two macrophage enhancer pathways in pre-B cells. Transcription-factor-induced somatic cell conversions are highly relevant for both basic and clinical research yet their mechanism is not fully understood and it is unclear whether they reflect normal differentiation processes. Here we show that during pre-B-cell-to-macrophage transdifferentiation, C/EBPα binds to two types of myeloid enhancers in B cells: pre-existing enhancers that are bound by PU.1, providing a platform for incoming C/EBPα; and de novo enhancers that are targeted by C/EBPα, acting as a pioneer factor for subsequent binding by PU.1. The order of factor binding dictates the upregulation kinetics of nearby genes. Pre-existing enhancers are broadly active throughout the hematopoietic lineage tree, including B cells. In contrast, de novo enhancers are silent in most cell types except in myeloid cells where they become activated by C/EBP factors. Our data suggest that C/EBPα recapitulates physiological developmental processes by short-circuiting two macrophage enhancer pathways in pre-B cells. [Display omitted] •C/EBPα activates two classes of prospective myeloid enhancers in B cells•Pre-existing enhancers are bound by PU.1 and become hyper-activated by C/EBPα•C/EBPα acts as a pioneer factor with delayed kinetics on de novo enhancers•The two types of enhancers direct myeloid cell fate in B cells and hematopoiesis In this study, Graf and colleagues show that, during B-cell-to-macrophage transdifferentiation, C/EBPα activates two types of myeloid enhancers in B cells. The two enhancer types are differentially activated, dictating gene expression levels of macrophage genes during the conversion of B cells into macrophages and normal hematopoiesis. |
| Author | Collombet, Samuel Badeaux, Aimee Bonifer, Constanze Sardina, Jose Luis van Oevelen, Chris Bussmann, Lars Beato, Miguel Hoogenkamp, Maarten Shi, Yang Vicent, Guillermo Lepoivre, Cyrille Graf, Thomas Thieffry, Denis |
| AuthorAffiliation | 2 Ecole Normale Supérieure, Institut de Biologie de l’ENS, INSERM, U1024, Centre National de la Recherche Scientifique (CNRS) 8197, 75005 Paris, France 1 Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain 4 CNRS, Aix-Marseille Université, IGS UMR7256, 13288 Marseille, France 3 School of Cancer Sciences, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK 5 Harvard Medical School, Children’s Hospital, Boston, MA 02115, USA |
| AuthorAffiliation_xml | – name: 2 Ecole Normale Supérieure, Institut de Biologie de l’ENS, INSERM, U1024, Centre National de la Recherche Scientifique (CNRS) 8197, 75005 Paris, France – name: 3 School of Cancer Sciences, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK – name: 1 Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain – name: 5 Harvard Medical School, Children’s Hospital, Boston, MA 02115, USA – name: 4 CNRS, Aix-Marseille Université, IGS UMR7256, 13288 Marseille, France |
| Author_xml | – sequence: 1 givenname: Chris surname: van Oevelen fullname: van Oevelen, Chris email: chris.vanoevelen@crg.eu organization: Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain – sequence: 2 givenname: Samuel surname: Collombet fullname: Collombet, Samuel organization: Ecole Normale Supérieure, Institut de Biologie de l’ENS, INSERM, U1024, Centre National de la Recherche Scientifique (CNRS) 8197, 75005 Paris, France – sequence: 3 givenname: Guillermo surname: Vicent fullname: Vicent, Guillermo organization: Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain – sequence: 4 givenname: Maarten surname: Hoogenkamp fullname: Hoogenkamp, Maarten organization: School of Cancer Sciences, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK – sequence: 5 givenname: Cyrille surname: Lepoivre fullname: Lepoivre, Cyrille organization: CNRS, Aix-Marseille Université, IGS UMR7256, 13288 Marseille, France – sequence: 6 givenname: Aimee surname: Badeaux fullname: Badeaux, Aimee organization: Harvard Medical School, Children’s Hospital, Boston, MA 02115, USA – sequence: 7 givenname: Lars surname: Bussmann fullname: Bussmann, Lars organization: Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain – sequence: 8 givenname: Jose Luis surname: Sardina fullname: Sardina, Jose Luis organization: Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain – sequence: 9 givenname: Denis surname: Thieffry fullname: Thieffry, Denis organization: Ecole Normale Supérieure, Institut de Biologie de l’ENS, INSERM, U1024, Centre National de la Recherche Scientifique (CNRS) 8197, 75005 Paris, France – sequence: 10 givenname: Miguel surname: Beato fullname: Beato, Miguel organization: Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain – sequence: 11 givenname: Yang surname: Shi fullname: Shi, Yang organization: Harvard Medical School, Children’s Hospital, Boston, MA 02115, USA – sequence: 12 givenname: Constanze surname: Bonifer fullname: Bonifer, Constanze organization: School of Cancer Sciences, Institute of Biomedical Research, University of Birmingham, Birmingham B15 2TT, UK – sequence: 13 givenname: Thomas surname: Graf fullname: Graf, Thomas email: thomas.graf@crg.eu organization: Center for Genomic Regulation and Pompeu Fabra University, 08003 Barcelona, Spain |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/26235892$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | B-Lymphocytes - cytology B-Lymphocytes - metabolism CCAAT-Enhancer-Binding Protein-alpha - genetics CCAAT-Enhancer-Binding Protein-alpha - metabolism Cell Line Cell Transdifferentiation Humans Myeloid Cells - cytology Myeloid Cells - metabolism Myelopoiesis Proto-Oncogene Proteins c-ets - genetics Proto-Oncogene Proteins c-ets - metabolism |
| Title | C/EBPα Activates Pre-existing and De Novo Macrophage Enhancers during Induced Pre-B Cell Transdifferentiation and Myelopoiesis |
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