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| Item Type: | Article |
|---|---|
| Title: | OCT4 acts as an integrator of pluripotency and signal-induced differentiation |
| Creators Name: | Simandi, Z., Horvath, A., Wright, L.C., Cuaranta-Monroy, I., De Luca, I., Karolyi, K., Sauer, S., Deleuze, J.F., Gudas, L.J., Cowley, S.M. and Nagy, L. |
| Abstract: | Cell type specification relies on the capacity of undifferentiated cells to properly respond to specific differentiation-inducing signals. Using genomic approaches along with loss- and gain-of-function genetic models, we identified OCT4-dependent mechanisms that provide embryonic stem cells with the means to customize their response to external cues. OCT4 binds a large set of low-accessible genomic regions. At these sites, OCT4 is required for proper enhancer and gene activation by recruiting co-regulators and RAR:RXR or {beta}-catenin, suggesting an unexpected collaboration between the lineage-determining transcription factor and these differentiation-initiating, signal-dependent transcription factors. As a proof of concept, we demonstrate that overexpression of OCT4 in a kidney cell line is sufficient for signal-dependent activation of otherwise unresponsive genes in these cells. Our results uncover OCT4 as an integral and necessary component of signal-regulated transcriptional processes required for tissue-specific responses. |
| Keywords: | Binding Sites, Cell Differentiation, Cell Lineage, Cellular Reprogramming, Embryonic Stem Cells, Gene Expression Regulation, Genetic Promoter Regions, Genetic Transcription, HEK293 Cells, Homeodomain Proteins, Octamer Transcription Factor-3, Pluripotent Stem Cells, RNA Interference, Retinoic Acid Receptor alpha, Retinoid X Receptors, Transfection, Tretinoin, Wnt Signaling Pathway, Animals, Mice |
| Source: | Molecular Cell |
| ISSN: | 1097-2765 |
| Publisher: | Cell Press / Elsevier |
| Volume: | 63 |
| Number: | 4 |
| Page Range: | 647-661 |
| Date: | 18 August 2016 |
| Official Publication: | https://doi.org/10.1016/j.molcel.2016.06.039 |
| PubMed: | View item in PubMed |
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