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Reconstructing divergent retinoid-induced cell fate-regulatory programs in stem cells [ChIP-Seq]

ABSTRACT: We have integrated dynamic RXRa binding, chromatin accessibility and promoter epigenetic status with the transcriptional activity inferred from RNA polymerase II mapping and transcription profiling. This demonstrated a temporal organization structure, in which early events are preferentially enriched for common GRNs, while cell fate specification is reflected by the activation of late programs in a cell-type specific manner. Furthermore, significant differences in cell lines' promoter status of genes associated with cell-line specific programs were inferred. Finally, a variety of transcription factors (TFs) playing a direct role in the signal transduction cascade downstream of the RXR/RAR initiated wiring were identified, several of them commonly regulated in both model systems, but in addition cell-type specific TF drivers were also identified.

ORGANISM(S): Mus musculus

PROVIDER: GSE68540 | GEO | 2016/09/15

SECONDARY ACCESSION(S): PRJNA283042

REPOSITORIES: GEO

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Reconstructing divergent retinoid-induced cell fate-regulatory programs in stem cells [Affymetrix]

Project description:We have integrated dynamic RXRa binding, chromatin accessibility and promoter epigenetic status with the transcriptional activity inferred from RNA polymerase II mapping and transcription profiling. This demonstrated a temporal organization structure, in which early events are preferentially enriched for common GRNs, while cell fate specification is reflected by the activation of late programs in a cell-type specific manner. Furthermore, significant differences in cell lines' promoter status of genes associated with cell-line specific programs were inferred. Finally, a variety of transcription factors (TFs) playing a direct role in the signal transduction cascade downstream of the RXR/RAR initiated wiring were identified, several of them commonly regulated in both model systems, but in addition cell-type specific TF drivers were also identified.

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Project description:Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors comprising retinoic acid (RARa,b,g) and retinoid X (RXRa,b,g) receptors. How a single signal induces highly complex temporally controlled networks that ultimately orchestrate physiological processes is unclear. Using an RA-inducible differentiation model we defined the temporal changes in the genome-wide binding patterns of RARg and RXRa and correlated them with transcription regulation. Unexpectedly, both receptors displayed a highly dynamic binding, with different RXRa heterodimers targeting identical loci. Comparison of RARg and RXRa co-binding at RA-regulated genes identified putative RXRa-RARg target genes that were validated with subtype-selective agonists. Gene regulatory decisions during differentiation were inferred from transcription factor target gene information and temporal gene expression. This analysis revealed 6 distinct co-expression paths of which RXRa-RARg is associated with transcription activation, while Sox2 and Egr1 were predicted to regulate repression. Finally, RXRa-RARg regulatory networks were reconstructed through integration of functional co-citations. Our analysis provides a dynamic view of RA signalling during cell differentiation, reveals RA heterodimer dynamics and promiscuity, and predicts decisions that diversify the RA signal into distinct gene-regulatory programs. Transcriptional activity in F9 cells treated with different retinoic acid receptor (RAR) agonists; like all-trans retinoic acid (ATRA), BMS961 (RARg-specific), BMS753 (RARa-specific) or BMS641(RARb-specific); has been evaluated at different time-points (2, 6, 24, 48h) and compared with that found under Ethanol-vehicle treatment conditions (48h treatment).

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Dissecting the retinoid-induced differentiation of F9 embryonal stem cells by integrative genomics [ChIP-seq]

Project description:Retinoic acid (RA) triggers physiological processes by activating heterodimeric transcription factors comprising retinoic acid (RARa,b,g) and retinoid X (RXRa,b,g) receptors. How a single signal induces highly complex temporally controlled networks that ultimately orchestrate physiological processes is unclear. Using an RA-inducible differentiation model we defined the temporal changes in the genome-wide binding patterns of RARg and RXRa and correlated them with transcription regulation. Unexpectedly, both receptors displayed a highly dynamic binding, with different RXRa heterodimers targeting identical loci. Comparison of RARg and RXRa co-binding at RA-regulated genes identified putative RXRa-RARg target genes that were validated with subtype-selective agonists. Gene regulatory decisions during differentiation were inferred from transcription factor target gene information and temporal gene expression. This analysis revealed 6 distinct co-expression paths of which RXRa-RARg is associated with transcription activation, while Sox2 and Egr1 were predicted to regulate repression. Finally, RXRa-RARg regulatory networks were reconstructed through integration of functional co-citations. Our analysis provides a dynamic view of RA signalling during cell differentiation, reveals RA heterodimer dynamics and promiscuity, and predicts decisions that diversify the RA signal into distinct gene-regulatory programs. RXRa; RARg and RNA Polymerase II chromatin binding has been assessed at five time points; in addition an input control for F9 cells as well as a RXRa ChIP-seq assay from a rxra-/- ko strain has been performed.

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Reconstructing divergent retinoid-induced cell fate-regulatory programs in stem cells

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Project description:This SuperSeries is composed of the SubSeries listed below.

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