Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates
The neuron-specific transcription factor Myt1l represses many somatic lineage programs, but not the neuronal lineage program, to both induce and maintain neuronal identity. Myt1L represses non-neuronal fates Lineage reprogramming by expression of transcription factors that modulate target cell fate...
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| Published in | Nature (London) Vol. 544; no. 7649; pp. 245 - 249 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
13.04.2017
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0028-0836 1476-4687 1476-4687 |
| DOI | 10.1038/nature21722 |
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| Abstract | The neuron-specific transcription factor Myt1l represses many somatic lineage programs, but not the neuronal lineage program, to both induce and maintain neuronal identity.
Myt1L represses non-neuronal fates
Lineage reprogramming by expression of transcription factors that modulate target cell fate program requires gene expression of the donor cell to be silenced. Given our current knowledge, we would expect that each reprogramming cocktail would need to differ for distinct cells of origin, but intriguingly this has not been the case experimentally so far. Marius Wernig and colleagues have found that the neuronal reprogramming factor Myt1l, which is expressed in all neurons, promotes neuronal fate in mice by repressing all other lineages during reprogramming from other cell types as well as during neurogenesis and in primary neurons. Their data suggests that changing epigenetic marks would not be sufficient to maintain a particular cell fate, and alternative lineages are actively repressed to confer neuronal identity.
Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs
1
,
2
. In reprogramming, the same factors are often used to reprogram many different donor cell types
3
. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors
4
,
5
, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l)
6
exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar ‘many-but-one’ lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types. |
|---|---|
| AbstractList | Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the same factors are often used to reprogram many different donor cell types. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar 'many-but-one' lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types. The neuron-specific transcription factor Myt1l represses many somatic lineage programs, but not the neuronal lineage program, to both induce and maintain neuronal identity. Myt1L represses non-neuronal fates Lineage reprogramming by expression of transcription factors that modulate target cell fate program requires gene expression of the donor cell to be silenced. Given our current knowledge, we would expect that each reprogramming cocktail would need to differ for distinct cells of origin, but intriguingly this has not been the case experimentally so far. Marius Wernig and colleagues have found that the neuronal reprogramming factor Myt1l, which is expressed in all neurons, promotes neuronal fate in mice by repressing all other lineages during reprogramming from other cell types as well as during neurogenesis and in primary neurons. Their data suggests that changing epigenetic marks would not be sufficient to maintain a particular cell fate, and alternative lineages are actively repressed to confer neuronal identity. Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs 1 , 2 . In reprogramming, the same factors are often used to reprogram many different donor cell types 3 . As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors 4 , 5 , it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) 6 exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar ‘many-but-one’ lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types. Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the same factors are often used to reprogram many different donor cell types. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar 'many-but-one' lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types.Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the same factors are often used to reprogram many different donor cell types. As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors, it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar 'many-but-one' lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types. Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs 1 , 2 . In reprogramming, the same factors are often used to reprogram many different donor cell types 3 . As most developmental repressors, such as RE1-silencing transcription factor (REST) and Groucho (also known as TLE), are considered lineage-specific repressors 4 , 5 , it remains unclear how identical combinations of transcription factors can silence so many different donor programs. Distinct lineage repressors would have to be induced in different donor cell types. Here, by studying the reprogramming of mouse fibroblasts to neurons, we found that the pan neuron-specific transcription factor Myt1-like (Myt1l) 6 exerts its pro-neuronal function by direct repression of many different somatic lineage programs except the neuronal program. The repressive function of Myt1l is mediated via recruitment of a complex containing Sin3b by binding to a previously uncharacterized N-terminal domain. In agreement with its repressive function, the genomic binding sites of Myt1l are similar in neurons and fibroblasts and are preferentially in an open chromatin configuration. The Notch signalling pathway is repressed by Myt1l through silencing of several members, including Hes1. Acute knockdown of Myt1l in the developing mouse brain mimicked a Notch gain-of-function phenotype, suggesting that Myt1l allows newborn neurons to escape Notch activation during normal development. Depletion of Myt1l in primary postmitotic neurons de-repressed non-neuronal programs and impaired neuronal gene expression and function, indicating that many somatic lineage programs are actively and persistently repressed by Myt1l to maintain neuronal identity. It is now tempting to speculate that similar ‘many-but-one’ lineage repressors exist for other cell fates; such repressors, in combination with lineage-specific activators, would be prime candidates for use in reprogramming additional cell types. |
| Audience | Academic |
| Author | Wernig, Marius Drake, Sienna Mall, Moritz Walker, Brandon M. Ahlenius, Henrik Vierbuchen, Thomas Brennecke, Philip Fuentes, Daniel R. Kareta, Michael S. Steinmetz, Lars M. Taipale, Jussi Zhou, Bo Südhof, Thomas C. Ge, Xuecai Euong Ang, Cheen Chanda, Soham Grieder, Sarah D. Perotti, Nicholas Nitta, Kazuhiro R. Jolma, Arttu |
| AuthorAffiliation | 2. Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute 8. Genome Scale Biology Program, University of Helsinki, 00014 Helsinki, Finland 12. Current Address: Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan 1. Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine 10. Current Address: Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA 3. Department of Genetics 4. Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA 5. Lund Stem Cell Center, Lund University, 221 84 Lund, Sweden 9. Current Address: Children’s Health Research Center, Sanford Research, Sioux Falls, SD 57104, USA 7. Genome Biology Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany 11. Current Address: Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany 6. Division of Functional Genomics and Systems Biology, Departm |
| AuthorAffiliation_xml | – name: 7. Genome Biology Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany – name: 5. Lund Stem Cell Center, Lund University, 221 84 Lund, Sweden – name: 4. Department of Developmental Biology, Stanford University, Stanford, CA 94305, USA – name: 10. Current Address: Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA – name: 2. Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute – name: 11. Current Address: Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany – name: 3. Department of Genetics – name: 9. Current Address: Children’s Health Research Center, Sanford Research, Sioux Falls, SD 57104, USA – name: 1. Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine – name: 8. Genome Scale Biology Program, University of Helsinki, 00014 Helsinki, Finland – name: 6. Division of Functional Genomics and Systems Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, 171 77 Stockholm, Sweden – name: 12. Current Address: Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan |
| Author_xml | – sequence: 1 givenname: Moritz surname: Mall fullname: Mall, Moritz organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University – sequence: 2 givenname: Michael S. surname: Kareta fullname: Kareta, Michael S. organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, †Present addresses: Genetics and Genomics Group, Sanford Research, Sioux Falls, SD 57104, USA (M.S.K.); Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA (X.G.); Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA (T.V.); Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany (P.B.); Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan (K.R.N.) – sequence: 3 givenname: Soham surname: Chanda fullname: Chanda, Soham organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University – sequence: 4 givenname: Henrik surname: Ahlenius fullname: Ahlenius, Henrik organization: Department of Clinical Sciences, Division of Neurology and Lund Stem Cell Center, Lund University – sequence: 5 givenname: Nicholas surname: Perotti fullname: Perotti, Nicholas organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University – sequence: 6 givenname: Bo surname: Zhou fullname: Zhou, Bo organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University – sequence: 7 givenname: Sarah D. surname: Grieder fullname: Grieder, Sarah D. organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University – sequence: 8 givenname: Xuecai surname: Ge fullname: Ge, Xuecai organization: Department of Developmental Biology, Stanford University, †Present addresses: Genetics and Genomics Group, Sanford Research, Sioux Falls, SD 57104, USA (M.S.K.); Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA (X.G.); Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA (T.V.); Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany (P.B.); Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan (K.R.N.) – sequence: 9 givenname: Sienna surname: Drake fullname: Drake, Sienna organization: Department of Clinical Sciences, Division of Neurology and Lund Stem Cell Center, Lund University – sequence: 10 givenname: Cheen surname: Euong Ang fullname: Euong Ang, Cheen organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University – sequence: 11 givenname: Brandon M. surname: Walker fullname: Walker, Brandon M. organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University – sequence: 12 givenname: Thomas surname: Vierbuchen fullname: Vierbuchen, Thomas organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, †Present addresses: Genetics and Genomics Group, Sanford Research, Sioux Falls, SD 57104, USA (M.S.K.); Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA (X.G.); Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA (T.V.); Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany (P.B.); Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan (K.R.N.) – sequence: 13 givenname: Daniel R. surname: Fuentes fullname: Fuentes, Daniel R. organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University – sequence: 14 givenname: Philip surname: Brennecke fullname: Brennecke, Philip organization: Department of Genetics, Stanford University, †Present addresses: Genetics and Genomics Group, Sanford Research, Sioux Falls, SD 57104, USA (M.S.K.); Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA (X.G.); Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA (T.V.); Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany (P.B.); Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan (K.R.N.) – sequence: 15 givenname: Kazuhiro R. surname: Nitta fullname: Nitta, Kazuhiro R. organization: Division of Functional Genomics and Systems Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, †Present addresses: Genetics and Genomics Group, Sanford Research, Sioux Falls, SD 57104, USA (M.S.K.); Molecular and Cellular Biology, University of California Merced, Merced, CA 95343, USA (X.G.); Department of Neurobiology, Harvard Medical School, Boston, Massachusetts 02115, USA (T.V.); Leibniz-Institute for Molecular Pharmacology, 13125 Berlin, Germany (P.B.); Division of Genomic Technologies, RIKEN Center for Life Science Technologies, Yokohama 230-0045, Japan (K.R.N.) – sequence: 16 givenname: Arttu surname: Jolma fullname: Jolma, Arttu organization: Division of Functional Genomics and Systems Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet – sequence: 17 givenname: Lars M. surname: Steinmetz fullname: Steinmetz, Lars M. organization: Department of Genetics, Stanford University, Genome Biology Unit, European Molecular Biology Laboratory (EMBL) – sequence: 18 givenname: Jussi surname: Taipale fullname: Taipale, Jussi organization: Division of Functional Genomics and Systems Biology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Genome Scale Biology Program, University of Helsinki – sequence: 19 givenname: Thomas C. surname: Südhof fullname: Südhof, Thomas C. organization: Department of Molecular and Cellular Physiology and Howard Hughes Medical Institute, Stanford University – sequence: 20 givenname: Marius surname: Wernig fullname: Wernig, Marius email: wernig@stanford.edu organization: Department of Pathology and Institute for Stem Cell Biology and Regenerative Medicine, Stanford University |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 14 content type line 23 M.M. was responsible for research design, execution, data analysis, and manuscript preparation. M.S.K. performed and designed the bioinformatics analysis and aided in manuscript preparation. S.C. and B.Z. performed the electrophysiological analysis. H.A. performed the NSC experiments and advised on research design and manuscript preparation. X.G., C.E.A. and S.D. performed in utero electroporations. N.P. aided in the biochemical interaction studies. S.G. performed the FACS analysis. T.V., B.M.W. and D.R.F. generated constructs. P.B. and L.S. performed the sequencing. K.R.N., A.J., and J.T. performed the SELEX. T.C.S. supported the research. M.W. was responsible for supervision and design of research, data interpretation, and manuscript preparation. Author Contributions |
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| Snippet | The neuron-specific transcription factor Myt1l represses many somatic lineage programs, but not the neuronal lineage program, to both induce and maintain... Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs. In reprogramming, the... Normal differentiation and induced reprogramming require the activation of target cell programs and silencing of donor cell programs 1 , 2 . In reprogramming,... |
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| Title | Myt1l safeguards neuronal identity by actively repressing many non-neuronal fates |
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