Abstract
We have previously shown that the inhibition of fibroblast growth factor (FGF) signaling induced endodermal gene expression in the animal cap and caused the expansion of the endodermal mass in Xenopus embryos. However, we still do not know whether or not the alteration of FGF signaling controls embryonic cell fate, or when FGF signal blocking is required for endoderm formation in Xenopus. Here, we show that FGF signal blocking in embryonic cells causes their descendants to move into the endodermal region and to express endodermal genes. It is also interesting that blocking FGF signaling between fertilization and embryonic stage 10.5 promotes endoderm formation, but persistent FGF signaling blocking after stage 10.5 restricts endoderm formation and differentiation.
Highlights
Embryonic cells that have just finished cell cleavage choose their fate among one of three germ layers depending on their maternally determined extraand intracellular environment
On the contrary, when wild type fibroblast growth factor (FGF) receptor (WT-FR) mRNA was injected into the A1 cell, its descendants were not seen in the endodermal location, but in the anterior or lateral epidermis and muscle (Figure 1C)
We showed that the blocking of FGF signaling caused descendants of the presumptive ectodermal cells, whose fate would not normally be endoderm, to distribute into the gut and the abdominal region of tailbud stage embryos
Summary
Embryonic cells that have just finished cell cleavage choose their fate among one of three germ layers depending on their maternally determined extraand intracellular environment. This process, called germ layer specification, is one of the rate-limiting events in vertebrate embryogenesis. In Xenopus, the signaling pathways of endoderm formation are activated by VegT, a maternally encoded T-box transcription factor. Several major pathways including canonical Wnt signaling, GATA factors, and Notch signaling activate endoderm specific genes, strongly suggesting the complexity of the molecular hierarchy in endoderm formation (Agius et al, 2000; Patient and McGhee, 2002; Hilton et al, 2003; Vincent et al, 2003; Kofron et al, 2004; Wardle and Smith, 2006)
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