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Post-transcriptional tuning of FGF signaling mediates neural crest induction

ABSTRACT: Ectodermal patterning is required for the establishment of multiple components of the vertebrate body plan. Previous studies have demonstrated that precise combinations of extracellular signals determine the induction of neural or neural crest progenitors. Yet, we still have a limited understanding of how the response to inductive signals is optimized to generate the proper transcriptional output in target cells. Here we show that post-transcriptional attenuation of signaling gradients is essential for the formation of the neural crest. We found that neural crest cells display enhanced expression of Dicer, which promotes the maturation of a set of cell-type-specific miRNAs. These miRNAs target multiple components of the FGF signaling pathway, a central player in the process of neural induction in avian embryos. Loss of neural crest miRNAs prevented the attenuation of this neuralizing signal, leading to the expansion of the neural plate at the expense of neural crest cells. Thus, the post-transcriptional attenuation of FGF signaling is pre-requisite for neural crest specification. These findings demonstrate how post-transcriptional repression may reshape signaling gradients to set the boundaries between distinct spatial domains of progenitor cells.

ORGANISM(S): Gallus gallus

PROVIDER: GSE150007 | GEO | 2020/12/07

REPOSITORIES: GEO

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Project description:This is the simple model without diffusion described in th epublication Sharp developmental thresholds defined through bistability by antagonistic gradients of retinoic acid and FGF signaling. Goldbeter A, Gonze D, Pourquié O. Dev Dyn. 2007 Jun;236(6):1495-508. PMID: 17497689, doi:10.1016/j.jtbi.2008.01.006 Abstract: The establishment of thresholds along morphogen gradients in the embryo is poorly understood. Using mathematical modeling, we show that mutually inhibitory gradients can generate and position sharp morphogen thresholds in the embryonic space. Taking vertebrate segmentation as a paradigm, we demonstrate that the antagonistic gradients of retinoic acid (RA) and Fibroblast Growth Factor (FGF) along the presomitic mesoderm (PSM) may lead to the coexistence of two stable steady states. Here, we propose that this bistability is associated with abrupt switches in the levels of FGF and RA signaling, which permit the synchronized activation of segmentation genes, such as mesp2, in successive cohorts of PSM cells in response to the segmentation clock, thereby defining the future segments. Bistability resulting from mutual inhibition of RA and FGF provides a molecular mechanism for the all-or-none transitions assumed in the "clock and wavefront" somitogenesis model. Given that mutually antagonistic signaling gradients are common in development, such bistable switches could represent an important principle underlying embryonic patterning. Originally created by libAntimony v1.4 (using libSBML 3.4.1) This model originates from BioModels Database: A Database of Annotated Published Models (http://www.ebi.ac.uk/biomodels/). It is copyright (c) 2005-2011 The BioModels.net Team. For more information see the terms of use. To cite BioModels Database, please use: Li C, Donizelli M, Rodriguez N, Dharuri H, Endler L, Chelliah V, Li L, He E, Henry A, Stefan MI, Snoep JL, Hucka M, Le Novère N, Laibe C (2010) BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. BMC Syst Biol., 4:92.

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Post-transcriptional tuning of FGF signaling mediates neural crest induction

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