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Core Transcriptional Regulatory Circuitry in Human Embryonic Stem Cells

Mapping Transcription Factor Occupancy in Human Embryonic Stem Cells

Data Oct4 Promoter Occupancy in Human ES Cells
Oct4, Sox2 and Nanog Co-occupy Many Target Genes
ES Cell Transcription Factors Occupy Active and Inactive Genes
Core Transcriptional Regulatory Circuitry in ES Cells
Expanded Transcriptional Regulatory Circuitry
Supplementary Information




Acknowledgements
References
Expanded Transcriptional Regulatory Circuitry

An initial model for ES cell transcriptional regulatory circuitry was constructed by identifying Oct4, Sox2, and Nanog target genes that encode transcription factors and chromatin regulators, and integrating knowledge of the functions of these downstream regulators in both human and mouse based on the available expression studies and literature (Figure 5). The model includes a set of active and a set of repressed target genes based on the extensive expression characterization of the 353 co-bound genes as described earlier. The active targets include genes encoding components of chromatin remodeling and histone modifying complexes (e.g. SMARCAD1, MYST3, and SET), which may have general roles in transcriptional regulation and genes encoding transcription factors (e.g. REST, SKIL, HESX1, STAT3) which themselves are known to regulate specific genes.

Core transcriptional regulatory network in human ES cells. A model for the core transcriptional regulatory network was constructed by identifying Oct4, Sox2, and Nanog target genes that encode transcription factors and chromatin regulators, and integrating knowledge of the functions of these downstream regulators based on comparison to multiple expression datasets and to the literature. Regulators are represented by blue circles; gene promoters are represented by red rectangles; grey boxes represent putative downstream target genes. Positive regulation was assumed if the target gene was expressed whereas negative regulation was assumed if the target gene was not transcribed.
 
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