Visualizing Long-Range Movement of the Morphogen Xnr2 in the Xenopus Embryo (original) (raw)

Spatial response to fibroblast growth factor signalling in Xenopus embryos

Development, 1999

We have examined the spatial pattern of activation of the extracellular signal-regulated protein kinase (ERK) during Xenopus development, and show that it closely resembles the expression of various fibroblast growth factors (FGFs). Until the tailbud stage of development, all ERK activation domains are sensitive to the dominant negative FGF receptor, showing that activation is generated by endogenous FGF signalling. ERK is not activated by application of other growth factors like BMP4 or activin, nor is endogenous activation blocked by the respective dominant negative receptors. This shows that various domains of FGF expression, including the periblastoporal region and the midbrain-hindbrain boundary, are also sites of FGF signalling in vivo. Wounding induces a transient (<60 minutes) activation of ERK which is not significantly reduced by the dominant negative FGF receptor. An artificial FGF source, created by injection of eFGF mRNA into cleavage stage embryos, provokes ERK acti...

Inhibition of FGF signaling converts dorsal mesoderm to ventral mesoderm in early Xenopus embryos

Differentiation, 2011

In early vertebrate development, mesoderm induction is a crucial event regulated by several factors including the activin, BMP and FGF signaling pathways. While the requirement of FGF in Nodal/activininduced mesoderm formation has been reported, the fate of the tissue modulated by these signals is not fully understood. Here, we examined the fate of tissues when exogenous activin was added and FGF signaling was inhibited in animal cap explants of Xenopus embryos. Activin-induced dorsal mesoderm was converted to ventral mesoderm by inhibition of FGF signaling. We also found that inhibiting FGF signaling in the dorsal marginal zone, in vegetal-animal cap conjugates or in the presence of the activin signaling component Smad2, converted dorsal mesoderm to ventral mesoderm. The expression and promoter activities of a BMP responsive molecule, PV.1 and a Spemann organizer, noggin, were investigated while FGF signaling was inhibited. PV.1 expression increased, while noggin decreased. In addition, inhibiting BMP-4 signaling abolished ventral mesoderm formation induced by exogenous activin and FGF inhibition. Taken together, these results suggest that the formation of dorso-ventral mesoderm in early Xenopus embryos is regulated by a combination of FGF, activin and BMP signaling.

The Xenopus Brachyury promoter is activated by FGF and low concentrations ofactivinandsuppressed by high concentrationsof activin and by paired-type homeodomain proteins

Genes & Development, 1997

The mesoderm of Xenopus laevis arises through an inductive interaction in which signals from the vegetal hemisphere of the embryo act on overlying equatorial cells. One candidate for an endogenous mesoderm-inducing factor is activin, a member of the TGF␤ superfamily. Activin is of particular interest because it induces different mesodermal cell types in a concentration-dependent manner, suggesting that it acts as a morphogen. These concentration-dependent effects are exemplified by the response of Xbra, expression of which is induced in ectodermal tissue by low concentrations of activin but not by high concentrations. Xbra therefore offers an excellent paradigm for studying the way in which a morphogen gradient is interpreted in vertebrate embryos. In this paper we examine the trancriptional regulation of Xbra2, a pseudoallele of Xbra that shows an identical response to activin. Our results indicate that 381 bp 5 of the Xbra2 transcription start site are sufficient to confer responsiveness both to FGF and, in a concentration-dependent manner, to activin. We present evidence that the suppression of Xbra expression at high concentrations of activin is mediated by paired-type homeobox genes such as goosecoid, Mix.1, and Xotx2.

eFGF is expressed in the dorsal midline of Xenopus laevis

The International journal of developmental biology, 1995

A detailed study of the expression pattern of embryonic fibroblast growth factor (eFGF) during early Xenopus development has been undertaken using whole-mount DIG in situ hybridization. We show that the zygotic expression of eFGF is activated in the mesoderm of the early gastrula and is first visualized as a ring around the blastopore, with significantly higher levels of expression on the dorsal side of the embryo. As gastrulation proceeds, eFGF transcripts become increasingly abundant in the dorsal blastopore lip. In the early neurula eFGF expression can be detected in the extreme posterior of the embryo around the closed blastopore and in the cells of the notochord. This latter result is significant and represents the first report of a Xenopus FGF that is expressed in the notochord. In addition, we show that during gastrula and neurula stages, expression of eFGF closely follows the expression of the Xenopus brachyury (Xbra) gene. During later development eFGF expression is localiz...

Activin as a morphogen in Xenopus mesoderm induction1

Seminars in Cell & Developmental Biology, 1999

Activin, a member of the Transforming Growth Factor beta ( ) TGF-␤ superfamily, can behave as a morphogen in cells of the early Xenopus embryo by inducing a range of mesodermal genes in a concentration-dependent manner. This review examines the behaviour of activin as it forms a morphogen gradient. It also discusses how a cell can perceive its position in a concentration gradient in order to activate appropriate mesodermal gene responses. Key words: activin r morphogen r mesoderm induction r Xenopus ᮊ1999 Academic Press ᮊ1999 Academic Press 1084-9521r 99 r 030311q 07 $30.00r 0

Inhibition of FGF signaling causes expansion of the endoderm in Xenopus

Biochemical and Biophysical Research Communications, 2004

Fibroblast growth factor (FGF) is established as an initiator of signaling events critical for neurogenesis and mesoderm formation during early Xenopus embryogenesis. However, less is known about the role FGF signaling plays in endoderm specification. Here, we show for the first time that endoderm-specific genes are induced when FGF signaling is blocked in animal cap explants. This block of FGF signaling is also responsible for a significant enhancement of endodermal gene expression in animal cap explants that are injected with a dominant-negative BMP-4 receptor (DNBR) RNA or treated with activin, however, neural and mesoderm gene expression is diminished. Consistent with these results, the injection of dominant-negative FGF receptor (DNFR) RNA expands endodermal cell fate boundaries while FGF treatment dramatically reduces endoderm in whole embryos. Taken together, these results indicate that inhibition of FGF signaling promotes endoderm formation, whereas the presence of active FGF signaling is necessary for neurogenesis/mesoderm formation.

Temporal and spatial expression of FGF ligands and receptors during Xenopus development

Developmental Dynamics, 2009

Fibroblast growth factor (FGF) signalling plays a major role during early vertebrate development. It is involved in the specification of the mesoderm, control of morphogenetic movements, patterning of the anterior-posterior axis, and neural induction. In mammals, 22 FGF ligands have been identified, which can be grouped into seven subfamilies according to their sequence homology and function. We have cloned 17 fgf genes from Xenopus tropicalis and have analysed their temporal expression by RT-PCR and spatial expression by whole mount in situ hybridisation at key developmental stages. It reveals the diverse expression pattern of fgf genes during early embryonic development. Furthermore, our analysis shows the transient nature of expression of several fgfs in a number of embryonic tissues. This study constitutes the most comprehensive description of the temporal and spatial expression pattern of fgf ligands and receptors during vertebrate development to date. Developmental Dynamics 238:1467–1479, 2009. © 2009 Wiley-Liss, Inc.