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Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex
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| Zeitschriftentitel: | Development |
|---|---|
| Personen und Körperschaften: | , , , , , , , |
| In: | Development, 2016 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
The Company of Biologists
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| Schlagwörter: |
| author_facet |
Miller, Anzy Ralser, Meryem Kloet, Susan L. Loos, Remco Nishinakamura, Ryuichi Bertone, Paul Vermeulen, Michiel Hendrich, Brian Miller, Anzy Ralser, Meryem Kloet, Susan L. Loos, Remco Nishinakamura, Ryuichi Bertone, Paul Vermeulen, Michiel Hendrich, Brian |
|---|---|
| author |
Miller, Anzy Ralser, Meryem Kloet, Susan L. Loos, Remco Nishinakamura, Ryuichi Bertone, Paul Vermeulen, Michiel Hendrich, Brian |
| spellingShingle |
Miller, Anzy Ralser, Meryem Kloet, Susan L. Loos, Remco Nishinakamura, Ryuichi Bertone, Paul Vermeulen, Michiel Hendrich, Brian Development Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex Developmental Biology Molecular Biology |
| author_sort |
miller, anzy |
| spelling |
Miller, Anzy Ralser, Meryem Kloet, Susan L. Loos, Remco Nishinakamura, Ryuichi Bertone, Paul Vermeulen, Michiel Hendrich, Brian 1477-9129 0950-1991 The Company of Biologists Developmental Biology Molecular Biology http://dx.doi.org/10.1242/dev.139113 <jats:p>Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Though it is reported to play an important role in embryonic stem cell self-renewal, whether it is an essential pluripotency factor has been disputed. Here we show that Sall4 is dispensable for ES cell pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ES cells but is not required for maintenance of the pluripotency gene regulatory network. While a proportion of Sall4 protein physically associates with the Nucleosome Remodelling and Deacetylase (NuRD) complex, Sall4 neither recruits NuRD to chromatin nor influences transcription via NuRD; rather free Sall4 protein regulates transcription independently of NuRD. We propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.</jats:p> Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex Development |
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| title |
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_unstemmed |
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_full |
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_fullStr |
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_full_unstemmed |
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_short |
Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_sort |
sall4 controls differentiation of pluripotent cells independently of the nucleosome remodelling and deacetylation (nurd) complex |
| topic |
Developmental Biology Molecular Biology |
| url |
http://dx.doi.org/10.1242/dev.139113 |
| publishDate |
2016 |
| physical |
|
| description |
<jats:p>Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Though it is reported to play an important role in embryonic stem cell self-renewal, whether it is an essential pluripotency factor has been disputed. Here we show that Sall4 is dispensable for ES cell pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ES cells but is not required for maintenance of the pluripotency gene regulatory network. While a proportion of Sall4 protein physically associates with the Nucleosome Remodelling and Deacetylase (NuRD) complex, Sall4 neither recruits NuRD to chromatin nor influences transcription via NuRD; rather free Sall4 protein regulates transcription independently of NuRD. We propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.</jats:p> |
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| author | Miller, Anzy, Ralser, Meryem, Kloet, Susan L., Loos, Remco, Nishinakamura, Ryuichi, Bertone, Paul, Vermeulen, Michiel, Hendrich, Brian |
| author_facet | Miller, Anzy, Ralser, Meryem, Kloet, Susan L., Loos, Remco, Nishinakamura, Ryuichi, Bertone, Paul, Vermeulen, Michiel, Hendrich, Brian, Miller, Anzy, Ralser, Meryem, Kloet, Susan L., Loos, Remco, Nishinakamura, Ryuichi, Bertone, Paul, Vermeulen, Michiel, Hendrich, Brian |
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| description | <jats:p>Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Though it is reported to play an important role in embryonic stem cell self-renewal, whether it is an essential pluripotency factor has been disputed. Here we show that Sall4 is dispensable for ES cell pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ES cells but is not required for maintenance of the pluripotency gene regulatory network. While a proportion of Sall4 protein physically associates with the Nucleosome Remodelling and Deacetylase (NuRD) complex, Sall4 neither recruits NuRD to chromatin nor influences transcription via NuRD; rather free Sall4 protein regulates transcription independently of NuRD. We propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.</jats:p> |
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| spelling | Miller, Anzy Ralser, Meryem Kloet, Susan L. Loos, Remco Nishinakamura, Ryuichi Bertone, Paul Vermeulen, Michiel Hendrich, Brian 1477-9129 0950-1991 The Company of Biologists Developmental Biology Molecular Biology http://dx.doi.org/10.1242/dev.139113 <jats:p>Sall4 is an essential transcription factor for early mammalian development and is frequently overexpressed in cancer. Though it is reported to play an important role in embryonic stem cell self-renewal, whether it is an essential pluripotency factor has been disputed. Here we show that Sall4 is dispensable for ES cell pluripotency. Sall4 is an enhancer-binding protein that prevents precocious activation of the neural gene expression programme in ES cells but is not required for maintenance of the pluripotency gene regulatory network. While a proportion of Sall4 protein physically associates with the Nucleosome Remodelling and Deacetylase (NuRD) complex, Sall4 neither recruits NuRD to chromatin nor influences transcription via NuRD; rather free Sall4 protein regulates transcription independently of NuRD. We propose a model whereby enhancer binding by Sall4 and other pluripotency-associated transcription factors is responsible for maintaining the balance between transcriptional programmes in pluripotent cells.</jats:p> Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex Development |
| spellingShingle | Miller, Anzy, Ralser, Meryem, Kloet, Susan L., Loos, Remco, Nishinakamura, Ryuichi, Bertone, Paul, Vermeulen, Michiel, Hendrich, Brian, Development, Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex, Developmental Biology, Molecular Biology |
| title | Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_full | Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_fullStr | Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_full_unstemmed | Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_short | Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| title_sort | sall4 controls differentiation of pluripotent cells independently of the nucleosome remodelling and deacetylation (nurd) complex |
| title_unstemmed | Sall4 controls differentiation of pluripotent cells independently of the Nucleosome Remodelling and Deacetylation (NuRD) complex |
| topic | Developmental Biology, Molecular Biology |
| url | http://dx.doi.org/10.1242/dev.139113 |