Abstract
Early vertebrate embryos possess cells with the potential to generate all embryonic cell types. While this pluripotency is progressively lost as cells become lineage restricted, Neural Crest cells retain broad developmental potential. Here, we provide novel insights into signals essential for both pluripotency and neural crest formation in Xenopus. We show that FGF signaling controls a subset of genes expressed by pluripotent blastula cells, and find a striking switch in the signaling cascades activated by FGF signaling as cells lose pluripotency and commence lineage restriction. Pluripotent cells display and require Map Kinase signaling, whereas PI3 Kinase/Akt signals increase as developmental potential is restricted, and are required for transit to certain lineage restricted states. Importantly, retaining a high Map Kinase/low Akt signaling profile is essential for establishing Neural Crest stem cells. These findings shed important light on the signal-mediated control of pluripotency and the molecular mechanisms governing genesis of Neural Crest.
Highlights
The evolutionary transition from simple chordate body plans to complex vertebrate body plans was driven by the acquisition of the Neural Crest, a unique stem cell population with broad, multi-germ layer developmental potential (Le Douarin and Kalcheim, 1999; Hall, 2000; Bronner and LeDouarin, 2012; Prasad et al, 2012)
FGF signaling is required for proper gene expression in pluripotent blastula cells Because FGF signaling is known to play a role in the establishment of the neural crest cell population at the neural plate border in Xenopus, and is linked to the control of pluripotency in mouse embryonic stem cells (mESCs), we sought to determine if these signals were required in the pluripotent animal pole cells of blastula stage embryos
We found that at blastula stages, when explanted cells are pluripotent, they strongly express FGF receptor 4 (FGFR4) (Figure 1b), as these cells transit to an epidermal state, FGFR4 expression is lost
Summary
The evolutionary transition from simple chordate body plans to complex vertebrate body plans was driven by the acquisition of the Neural Crest, a unique stem cell population with broad, multi-germ layer developmental potential (Le Douarin and Kalcheim, 1999; Hall, 2000; Bronner and LeDouarin, 2012; Prasad et al, 2012). Models for how neural crest cells acquire their remarkably broad potential proposed that inductive interactions orchestrated by BMP, FGF, and Wnt signals endowed these cells with greater potency than the cells they were derived from developmentally or evolutionarily (Huang and Saint-Jeannet, 2004; Taylor and LaBonne, 2007; Prasad et al, 2012; Rogers et al, 2012; Stuhlmiller and Garcıa-Castro, 2012a). Such a mechanism conflicts, with the generalized view of embryonic development as a progressive restriction of developmental potential.
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