Genome-wide Kinase-Chromatin Interactions Reveal the Regulatory Network of ERK 
Signaling in Human Embryonic Stem Cells

Göke, J.; Chan, Y. S.; Yan, J. L.; Vingron, M.; Ng, H. H.

doi:DOI 10.1016/j.molcel.2013.04.030

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Genome-wide Kinase-Chromatin Interactions Reveal the Regulatory Network of ERK Signaling in Human Embryonic Stem Cells

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Göke, J.
Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Vingron, M.
Gene regulation (Martin Vingron), Dept. of Computational Molecular Biology (Head: Martin Vingron), Max Planck Institute for Molecular Genetics, Max Planck Society;

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Göke, J., Chan, Y. S., Yan, J. L., Vingron, M., & Ng, H. H. (2013). Genome-wide Kinase-Chromatin Interactions Reveal the Regulatory Network of ERK Signaling in Human Embryonic Stem Cells. Molecular Cell, 50(6), 844-855. doi:DOI 10.1016/j.molcel.2013.04.030.

Cite as: https://hdl.handle.net/11858/00-001M-0000-0019-0B22-F

Abstract

The extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase signal-transduction cascade is one of the key pathways regulating proliferation and differentiation in development and disease. ERK signaling is required for human embryonic stem cells' (hESCs') self-renewing property. Here, we studied the convergence of the ERK signaling cascade at the DNA by mapping genome-wide kinase-chromatin interactions for ERK2 in hESCs. We observed that ERK2 binding occurs near noncoding genes and histone, cell-cycle, metabolism, and pluripotency-associated genes. We find that the transcription factor ELK1 is essential in hESCs and that ERK2 co-occupies promoters bound by ELK1. Strikingly, promoters bound by ELK1 without ERK2 are occupied by Polycomb group proteins that repress genes involved in lineage commitment. In summary, we propose a model wherein extracellular-signaling-stimulated proliferation and intrinsic repression of differentiation are integrated to maintain the identity of hESCs.