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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 |
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| Personen und Körperschaften: | , , , , , , , |
| In: | Development, 2016 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
The Company of Biologists
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| Schlagwörter: |
| Zusammenfassung: | <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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| ISSN: |
1477-9129
0950-1991 |
| DOI: | 10.1242/dev.139113 |