SCL/TAL1 cooperates with Polycomb RYBP-PRC1 to suppress alternative lineages in blood-fated cells

During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood ( Scl/Tal1 ),...

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Published in:Nature communications Vol. 9; no. 1; pp. 5375 - 17
Main Authors: Chagraoui, Hedia, Kristiansen, Maiken S., Ruiz, Juan Pablo, Serra-Barros, Ana, Richter, Johanna, Hall-Ponselé, Elisa, Gray, Nicki, Waithe, Dominic, Clark, Kevin, Hublitz, Philip, Repapi, Emmanouela, Otto, Georg, Sopp, Paul, Taylor, Stephen, Thongjuea, Supat, Vyas, Paresh, Porcher, Catherine
Format: Journal Article
Language:English
Published: London Nature Publishing Group UK 18.12.2018
Nature Publishing Group
Nature Portfolio
Subjects:
14
14/19
45
45/100
45/15
45/41
45/47
45/91
631/136/232
631/337/176/2016
631/337/572
Animals
Blood
Cell Differentiation - physiology
Cell fate
Cell Line
Cell Lineage - physiology
Cell Separation - methods
Embryo, Mammalian
Embryonic growth stage
Flow Cytometry - methods
Gene expression
Gene Expression Regulation, Developmental - physiology
Gene silencing
Genomes
Heart
Histone Code - physiology
Humanities and Social Sciences
Mesoderm
Mesoderm - cytology
Mesoderm - physiology
Mice
Mouse Embryonic Stem Cells
multidisciplinary
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Phenotypes
Polycomb group proteins
Polycomb Repressive Complex 1 - metabolism
Polycomb-Group Proteins - metabolism
Repressor Proteins - genetics
Repressor Proteins - metabolism
RNA, Small Interfering - metabolism
Science
Science (multidisciplinary)
Specifications
T-Cell Acute Lymphocytic Leukemia Protein 1 - genetics
T-Cell Acute Lymphocytic Leukemia Protein 1 - metabolism
Transcription factors
Transcription Factors - genetics
Transcription Factors - metabolism
ISSN:2041-1723, 2041-1723
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Abstract During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood ( Scl/Tal1 ), cardiac ( Mesp1 ) and paraxial ( Tbx6 ) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl -null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes. Mechanisms that operate during embryonic development to restrict cell fate are currently under investigation. Here the authors characterise the role of SCL/TAL1 at the onset of blood specification in embryonic development using mouse EB differentiation culture as a model system.
AbstractList During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood (Scl/Tal1), cardiac (Mesp1) and paraxial (Tbx6) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl-null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes. Mechanisms that operate during embryonic development to restrict cell fate are currently under investigation. Here the authors characterise the role of SCL/TAL1 at the onset of blood specification in embryonic development using mouse EB differentiation culture as a model system.
During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood ( Scl/Tal1 ), cardiac ( Mesp1 ) and paraxial ( Tbx6 ) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl -null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes. Mechanisms that operate during embryonic development to restrict cell fate are currently under investigation. Here the authors characterise the role of SCL/TAL1 at the onset of blood specification in embryonic development using mouse EB differentiation culture as a model system.
During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood (Scl/Tal1), cardiac (Mesp1) and paraxial (Tbx6) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl-null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes.During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood (Scl/Tal1), cardiac (Mesp1) and paraxial (Tbx6) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl-null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes.
During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood (Scl/Tal1), cardiac (Mesp1) and paraxial (Tbx6) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl-null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes.
During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell fate. Here we investigate how mesoderm specifies into blood-fated cells. We document temporally restricted co-expression of blood ( Scl/Tal1 ), cardiac ( Mesp1 ) and paraxial ( Tbx6 ) lineage-affiliated transcription factors in single cells, at the onset of blood specification, supporting the existence of common progenitors. At the same time-restricted stage, absence of SCL results in expansion of cardiac/paraxial cell populations and increased cardiac/paraxial gene expression, suggesting active suppression of alternative fates. Indeed, SCL normally activates expression of co-repressor ETO2 and Polycomb-PRC1 subunits (RYBP, PCGF5) and maintains levels of Polycomb-associated histone marks (H2AK119ub/H3K27me3). Genome-wide analyses reveal ETO2 and RYBP co-occupy most SCL target genes, including cardiac/paraxial loci. Reduction of Eto2 or Rybp expression mimics Scl -null cardiac phenotype. Therefore, SCL-mediated transcriptional repression prevents mis-specification of blood-fated cells, establishing active repression as central to fate determination processes.
Mechanisms that operate during embryonic development to restrict cell fate are currently under investigation. Here the authors characterise the role of SCL/TAL1 at the onset of blood specification in embryonic development using mouse EB differentiation culture as a model system.
ArticleNumber 5375
Author Chagraoui, Hedia
Vyas, Paresh
Kristiansen, Maiken S.
Richter, Johanna
Hublitz, Philip
Taylor, Stephen
Gray, Nicki
Thongjuea, Supat
Ruiz, Juan Pablo
Hall-Ponselé, Elisa
Sopp, Paul
Serra-Barros, Ana
Porcher, Catherine
Otto, Georg
Repapi, Emmanouela
Waithe, Dominic
Clark, Kevin
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BackLink https://www.ncbi.nlm.nih.gov/pubmed/30560907$$D View this record in MEDLINE/PubMed
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Snippet During development, it is unclear if lineage-fated cells derive from multilineage-primed progenitors and whether active mechanisms operate to restrict cell...
Mechanisms that operate during embryonic development to restrict cell fate are currently under investigation. Here the authors characterise the role of...
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StartPage 5375
SubjectTerms 14
14/19
45
45/100
45/15
45/41
45/47
45/91
631/136/232
631/337/176/2016
631/337/572
Animals
Blood
Cell Differentiation - physiology
Cell fate
Cell Line
Cell Lineage - physiology
Cell Separation - methods
Embryo, Mammalian
Embryonic growth stage
Flow Cytometry - methods
Gene expression
Gene Expression Regulation, Developmental - physiology
Gene silencing
Genomes
Heart
Histone Code - physiology
Humanities and Social Sciences
Mesoderm
Mesoderm - cytology
Mesoderm - physiology
Mice
Mouse Embryonic Stem Cells
multidisciplinary
Nuclear Proteins - genetics
Nuclear Proteins - metabolism
Phenotypes
Polycomb group proteins
Polycomb Repressive Complex 1 - metabolism
Polycomb-Group Proteins - metabolism
Repressor Proteins - genetics
Repressor Proteins - metabolism
RNA, Small Interfering - metabolism
Science
Science (multidisciplinary)
Specifications
T-Cell Acute Lymphocytic Leukemia Protein 1 - genetics
T-Cell Acute Lymphocytic Leukemia Protein 1 - metabolism
Transcription factors
Transcription Factors - genetics
Transcription Factors - metabolism
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Title SCL/TAL1 cooperates with Polycomb RYBP-PRC1 to suppress alternative lineages in blood-fated cells
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